Ignet

Gene Information

Gene symbol: KLRK1

Gene name: killer cell lectin-like receptor subfamily K, member 1

HGNC ID: 18788

Synonyms: NKG2D, KLR, NKG2-D, CD314

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ATM	1 hits
3	ATR	1 hits
4	BCL2	1 hits
5	BIRC5	1 hits
6	C8orf4	1 hits
7	CCR5	1 hits
8	CCR7	1 hits
9	CD226	1 hits
10	CD28	1 hits
11	CD4	1 hits
12	CD40	1 hits
13	CD80	1 hits
14	CD81	1 hits
15	CD8A	1 hits
16	CSF1	1 hits
17	CSF2	1 hits
18	CTLA4	1 hits
19	CXCR3	1 hits
20	EGF	1 hits
21	EOMES	1 hits
22	FCGR3A	1 hits
23	HCST	1 hits
24	HLA-A	1 hits
25	HLA-B	1 hits
26	IFNG	1 hits
27	IL15	1 hits
28	IL15RA	1 hits
29	IL2	1 hits
30	IRF3	1 hits
31	ITGAM	1 hits
32	KIR2DL4	1 hits
33	KIR2DS2	1 hits
34	KLRC1	1 hits
35	KLRC2	1 hits
36	KLRG1	1 hits
37	MICA	1 hits
38	MICB	1 hits
39	NCAM1	1 hits
40	NCR1	1 hits
41	NCR3	1 hits
42	P4HB	1 hits
43	PDIA6	1 hits
44	RAE1	1 hits
45	SH2D1B	1 hits
46	TBK1	1 hits
47	TGFB1	1 hits

Related Sentences

#	PMID	Sentence
1	11557981	Rae1 and H60 ligands of the NKG2D receptor stimulate tumour immunity.
2	11557981	The stimulatory lectin-like NKG2D receptor is expressed by NK cells, activated CD8+ T cells and by activated macrophages in mice.
3	11557981	Mice that are exposed to live or irradiated tumour cells expressing Rae1 or H60 are specifically immune to subsequent challenge with tumour cells that lack NKG2D ligands, suggesting application of the ligands in the design of tumour vaccines.
4	11557981	Rae1 and H60 ligands of the NKG2D receptor stimulate tumour immunity.
5	11557981	The stimulatory lectin-like NKG2D receptor is expressed by NK cells, activated CD8+ T cells and by activated macrophages in mice.
6	11557981	Mice that are exposed to live or irradiated tumour cells expressing Rae1 or H60 are specifically immune to subsequent challenge with tumour cells that lack NKG2D ligands, suggesting application of the ligands in the design of tumour vaccines.
7	11557981	Rae1 and H60 ligands of the NKG2D receptor stimulate tumour immunity.
8	11557981	The stimulatory lectin-like NKG2D receptor is expressed by NK cells, activated CD8+ T cells and by activated macrophages in mice.
9	11557981	Mice that are exposed to live or irradiated tumour cells expressing Rae1 or H60 are specifically immune to subsequent challenge with tumour cells that lack NKG2D ligands, suggesting application of the ligands in the design of tumour vaccines.
10	14695218	MICA/NKG2D-mediated immunogene therapy of experimental gliomas.
11	14695218	Tumor cells expressing ligands of the activating immunoreceptor NKG2D stimulate tumor immunity mediated by natural killer (NK), gammadelta T, and CD8(+) T cells.
12	14695218	We report that human glioma cells express the NKG2D ligands MICA, MICB, and members of the UL16-binding protein family constitutively.
13	14695218	However, glioma cells resist NK cell cytolysis because of high MHC class I antigen expression.
14	14695218	MICA/NKG2D-mediated immunogene therapy of experimental gliomas.
15	14695218	Tumor cells expressing ligands of the activating immunoreceptor NKG2D stimulate tumor immunity mediated by natural killer (NK), gammadelta T, and CD8(+) T cells.
16	14695218	We report that human glioma cells express the NKG2D ligands MICA, MICB, and members of the UL16-binding protein family constitutively.
17	14695218	However, glioma cells resist NK cell cytolysis because of high MHC class I antigen expression.
18	14695218	MICA/NKG2D-mediated immunogene therapy of experimental gliomas.
19	14695218	Tumor cells expressing ligands of the activating immunoreceptor NKG2D stimulate tumor immunity mediated by natural killer (NK), gammadelta T, and CD8(+) T cells.
20	14695218	We report that human glioma cells express the NKG2D ligands MICA, MICB, and members of the UL16-binding protein family constitutively.
21	14695218	However, glioma cells resist NK cell cytolysis because of high MHC class I antigen expression.
22	15607810	DC1 induction depends on NK cell-produced IFN-gamma and TNF-alpha, with a possible involvement of additional factors.
23	15607810	While NKG2D-dependent tumor cell recognition is sufficient to induce the cytotoxic "effector" function of NK cells, the induction of "NK cell help" requires additional signals from type-1 IFNs, products of virally-infected cells, or from IL-2.
24	15867395	Increased NK activity was associated with a raise in CD3-CD56+ NK and/or CD3+CD56+ NK-like T cells, displaying enhanced expression of NKG2D and/or NKp46 receptors.
25	15867395	Up-regulated expression of CD83 and CD40 and increased interleukin-12 release on stimulation were observed in CD14+ cells from post-HSP96 peripheral blood mononuclear cells, suggesting an indirect pathway of NK stimulation by HSP96-activated monocytes.
26	15879099	Tat-induced TGF-beta mRNA synthesis is also blocked by the ERK1 inhibitor PD98059, suggesting that ERK1 is needed for TGF-beta production.
27	15879099	Moreover, Tat strongly activates the c-Jun component of the multimolecular complex AP-1, whereas TGF-beta triggers c-Fos and c-Jun.
28	15879099	Of note, treatment of NK cells with PTX-B or PT9K/129G inhibits Tat- and TGF-beta-induced activation of AP-1.
29	15879099	TGF-beta enhances starvation-induced NK cell apoptosis, significantly reduces transcription of the antiapoptotic protein Bcl-2, and inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D.
30	15879099	It is of note that in NK cells from patients with early HIV-1 infection, mRNA expression of Bcl-2 and Bcl-x(L) was consistently lower than that in healthy donors; interestingly, TGF-beta and Tat were detected in the sera of these patients.
31	15919373	The majority of these cells co-express CD16, CD11b, NKG2D, and NKp46.
32	16040807	The interaction of NKG2D, a stimulatory receptor expressed on natural killer (NK) cells and activated CD8(+) T cells, and its ligands mediates stimulatory and costimulatory signals to these cells.
33	16040807	Here, we demonstrate that DNA-based vaccines, encoding syngeneic or allogeneic NKG2D ligands together with tumor antigens such as survivin or carcinoembryonic antigen, markedly activate both innate and adaptive antitumor immunity.
34	16040807	The interaction of NKG2D, a stimulatory receptor expressed on natural killer (NK) cells and activated CD8(+) T cells, and its ligands mediates stimulatory and costimulatory signals to these cells.
35	16040807	Here, we demonstrate that DNA-based vaccines, encoding syngeneic or allogeneic NKG2D ligands together with tumor antigens such as survivin or carcinoembryonic antigen, markedly activate both innate and adaptive antitumor immunity.
36	16210663	Levels of expression of NK-activating receptor NKG2D and CD16 on NK cell surface were assayed in the vaccinated mice.
37	16210663	Expression of NKG2D ligands, Rae1, and H60 on SCC VII/SF cells was also examined.
38	16210663	NK cells from tumor-bearing mice expressed significantly lower levels of NKG2D and CD16 compared with rvv-IL-2 vaccinated mice.
39	16210663	Incubation of NK cells with tumor homogenate or cultured supernatant of SCC VII/SF cells reduced the expression of NKG2D and CD16.
40	16210663	SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells.
41	16210663	Levels of expression of NK-activating receptor NKG2D and CD16 on NK cell surface were assayed in the vaccinated mice.
42	16210663	Expression of NKG2D ligands, Rae1, and H60 on SCC VII/SF cells was also examined.
43	16210663	NK cells from tumor-bearing mice expressed significantly lower levels of NKG2D and CD16 compared with rvv-IL-2 vaccinated mice.
44	16210663	Incubation of NK cells with tumor homogenate or cultured supernatant of SCC VII/SF cells reduced the expression of NKG2D and CD16.
45	16210663	SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells.
46	16210663	Levels of expression of NK-activating receptor NKG2D and CD16 on NK cell surface were assayed in the vaccinated mice.
47	16210663	Expression of NKG2D ligands, Rae1, and H60 on SCC VII/SF cells was also examined.
48	16210663	NK cells from tumor-bearing mice expressed significantly lower levels of NKG2D and CD16 compared with rvv-IL-2 vaccinated mice.
49	16210663	Incubation of NK cells with tumor homogenate or cultured supernatant of SCC VII/SF cells reduced the expression of NKG2D and CD16.
50	16210663	SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells.
51	16210663	Levels of expression of NK-activating receptor NKG2D and CD16 on NK cell surface were assayed in the vaccinated mice.
52	16210663	Expression of NKG2D ligands, Rae1, and H60 on SCC VII/SF cells was also examined.
53	16210663	NK cells from tumor-bearing mice expressed significantly lower levels of NKG2D and CD16 compared with rvv-IL-2 vaccinated mice.
54	16210663	Incubation of NK cells with tumor homogenate or cultured supernatant of SCC VII/SF cells reduced the expression of NKG2D and CD16.
55	16210663	SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells.
56	16210663	Levels of expression of NK-activating receptor NKG2D and CD16 on NK cell surface were assayed in the vaccinated mice.
57	16210663	Expression of NKG2D ligands, Rae1, and H60 on SCC VII/SF cells was also examined.
58	16210663	NK cells from tumor-bearing mice expressed significantly lower levels of NKG2D and CD16 compared with rvv-IL-2 vaccinated mice.
59	16210663	Incubation of NK cells with tumor homogenate or cultured supernatant of SCC VII/SF cells reduced the expression of NKG2D and CD16.
60	16210663	SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells.
61	16273350	DC enhances NK activity in vitro, partly by sustaining NK cell survival and by enhancing the expression of NK-activating receptors, including NKp46 and NKG2D.
62	16273350	NKp46 and NKG2D expression showed a good correlation with the patients' NK activity.
63	16273350	DC enhances NK activity in vitro, partly by sustaining NK cell survival and by enhancing the expression of NK-activating receptors, including NKp46 and NKG2D.
64	16273350	NKp46 and NKG2D expression showed a good correlation with the patients' NK activity.
65	16368879	The NKG2D receptor is a stimulatory receptor expressed on NK cells and activated CD8 T cells.
66	16368879	We previously demonstrated that engaging the NKG2D receptor markedly improved the efficacy of a survivin-based DNA vaccine.
67	16368879	The combination vaccine, encoding both the NKG2D ligand H60 and survivin, activates innate and adaptive antitumor immunity and results in better protection against tumors of different origin and NKG2D expression levels.
68	16368879	However, depletion of CD4 T cells results in the activation of DCs, NK cells, and CD8 T cells and enhances NK cell activity.
69	16368879	The pH60/Survivin vaccine also increases DCs and NK cells but decreases CD4 T cell homing to Peyer patches, presumably as a result of changes in the homing receptor profile.
70	16368879	The NKG2D receptor is a stimulatory receptor expressed on NK cells and activated CD8 T cells.
71	16368879	We previously demonstrated that engaging the NKG2D receptor markedly improved the efficacy of a survivin-based DNA vaccine.
72	16368879	The combination vaccine, encoding both the NKG2D ligand H60 and survivin, activates innate and adaptive antitumor immunity and results in better protection against tumors of different origin and NKG2D expression levels.
73	16368879	However, depletion of CD4 T cells results in the activation of DCs, NK cells, and CD8 T cells and enhances NK cell activity.
74	16368879	The pH60/Survivin vaccine also increases DCs and NK cells but decreases CD4 T cell homing to Peyer patches, presumably as a result of changes in the homing receptor profile.
75	16368879	The NKG2D receptor is a stimulatory receptor expressed on NK cells and activated CD8 T cells.
76	16368879	We previously demonstrated that engaging the NKG2D receptor markedly improved the efficacy of a survivin-based DNA vaccine.
77	16368879	The combination vaccine, encoding both the NKG2D ligand H60 and survivin, activates innate and adaptive antitumor immunity and results in better protection against tumors of different origin and NKG2D expression levels.
78	16368879	However, depletion of CD4 T cells results in the activation of DCs, NK cells, and CD8 T cells and enhances NK cell activity.
79	16368879	The pH60/Survivin vaccine also increases DCs and NK cells but decreases CD4 T cell homing to Peyer patches, presumably as a result of changes in the homing receptor profile.
80	16552713	The hepatitis C virus (HCV) binds to human cells through the interaction of its envelope glycoprotein E2 with the tetraspanin CD81.
81	16552713	We have previously reported that engagement of CD81 has opposite effects on T and NK cell function, as it enhances T cell receptor-mediated T cell activation and inhibits CD16- or IL-12-mediated NK cell activation.
82	16552713	We further investigated this dichotomy and found that another tetraspanin, CD82, induces the same opposing effects on human primary T and NK cells.
83	16552713	Activation by other unrelated stimuli such as NKG2D- and beta-1 integrin is also reduced by CD81 ligation on NK cells.
84	16619285	Interleukin-15 mediates protection against experimental tuberculosis: a role for NKG2D-dependent effector mechanisms of CD8+ T cells.
85	16619285	Because IL-15 is important for the homeostasis of CD8+ T cells, we studied the immune response in IL-15-deficient mice during tuberculosis.
86	16619285	In the absence of IL-15, CD8+ T cells failed to efficiently accumulate in draining lymph nodes and at the site of infection.
87	16619285	The expression of antigen-specific effector functions, such as the production of interferon-gamma and cytotoxicity, were impaired in CD8+ T cells, but not CD4+ T cells, from IL-15-deficient mice.
88	16619285	The lectin-like stimulatory receptor natural killer group 2D (NKG2D) was up-regulated on CD8+ T cells only from wild-type mice, but not from IL-15-deficient mice.
89	16619285	Mechanistically, blocking NKG2D function with an mAb inhibited M. tuberculosis-directed CD8+ T cell responses in vitro.
90	16619285	We conclude that in addition to regulating the expansion of CD8+ T cells, IL-15 is also necessary for inducing effector mechanisms in CD8+ T cells that depend on NKG2D expression.
91	16619285	Hence, our results implicate IL-15 and NKG2D as promising targets for modulating CD8+ T cell-mediated protection against tuberculosis.
92	16619285	Interleukin-15 mediates protection against experimental tuberculosis: a role for NKG2D-dependent effector mechanisms of CD8+ T cells.
93	16619285	Because IL-15 is important for the homeostasis of CD8+ T cells, we studied the immune response in IL-15-deficient mice during tuberculosis.
94	16619285	In the absence of IL-15, CD8+ T cells failed to efficiently accumulate in draining lymph nodes and at the site of infection.
95	16619285	The expression of antigen-specific effector functions, such as the production of interferon-gamma and cytotoxicity, were impaired in CD8+ T cells, but not CD4+ T cells, from IL-15-deficient mice.
96	16619285	The lectin-like stimulatory receptor natural killer group 2D (NKG2D) was up-regulated on CD8+ T cells only from wild-type mice, but not from IL-15-deficient mice.
97	16619285	Mechanistically, blocking NKG2D function with an mAb inhibited M. tuberculosis-directed CD8+ T cell responses in vitro.
98	16619285	We conclude that in addition to regulating the expansion of CD8+ T cells, IL-15 is also necessary for inducing effector mechanisms in CD8+ T cells that depend on NKG2D expression.
99	16619285	Hence, our results implicate IL-15 and NKG2D as promising targets for modulating CD8+ T cell-mediated protection against tuberculosis.
100	16619285	Interleukin-15 mediates protection against experimental tuberculosis: a role for NKG2D-dependent effector mechanisms of CD8+ T cells.
101	16619285	Because IL-15 is important for the homeostasis of CD8+ T cells, we studied the immune response in IL-15-deficient mice during tuberculosis.
102	16619285	In the absence of IL-15, CD8+ T cells failed to efficiently accumulate in draining lymph nodes and at the site of infection.
103	16619285	The expression of antigen-specific effector functions, such as the production of interferon-gamma and cytotoxicity, were impaired in CD8+ T cells, but not CD4+ T cells, from IL-15-deficient mice.
104	16619285	The lectin-like stimulatory receptor natural killer group 2D (NKG2D) was up-regulated on CD8+ T cells only from wild-type mice, but not from IL-15-deficient mice.
105	16619285	Mechanistically, blocking NKG2D function with an mAb inhibited M. tuberculosis-directed CD8+ T cell responses in vitro.
106	16619285	We conclude that in addition to regulating the expansion of CD8+ T cells, IL-15 is also necessary for inducing effector mechanisms in CD8+ T cells that depend on NKG2D expression.
107	16619285	Hence, our results implicate IL-15 and NKG2D as promising targets for modulating CD8+ T cell-mediated protection against tuberculosis.
108	16619285	Interleukin-15 mediates protection against experimental tuberculosis: a role for NKG2D-dependent effector mechanisms of CD8+ T cells.
109	16619285	Because IL-15 is important for the homeostasis of CD8+ T cells, we studied the immune response in IL-15-deficient mice during tuberculosis.
110	16619285	In the absence of IL-15, CD8+ T cells failed to efficiently accumulate in draining lymph nodes and at the site of infection.
111	16619285	The expression of antigen-specific effector functions, such as the production of interferon-gamma and cytotoxicity, were impaired in CD8+ T cells, but not CD4+ T cells, from IL-15-deficient mice.
112	16619285	The lectin-like stimulatory receptor natural killer group 2D (NKG2D) was up-regulated on CD8+ T cells only from wild-type mice, but not from IL-15-deficient mice.
113	16619285	Mechanistically, blocking NKG2D function with an mAb inhibited M. tuberculosis-directed CD8+ T cell responses in vitro.
114	16619285	We conclude that in addition to regulating the expansion of CD8+ T cells, IL-15 is also necessary for inducing effector mechanisms in CD8+ T cells that depend on NKG2D expression.
115	16619285	Hence, our results implicate IL-15 and NKG2D as promising targets for modulating CD8+ T cell-mediated protection against tuberculosis.
116	16619285	Interleukin-15 mediates protection against experimental tuberculosis: a role for NKG2D-dependent effector mechanisms of CD8+ T cells.
117	16619285	Because IL-15 is important for the homeostasis of CD8+ T cells, we studied the immune response in IL-15-deficient mice during tuberculosis.
118	16619285	In the absence of IL-15, CD8+ T cells failed to efficiently accumulate in draining lymph nodes and at the site of infection.
119	16619285	The expression of antigen-specific effector functions, such as the production of interferon-gamma and cytotoxicity, were impaired in CD8+ T cells, but not CD4+ T cells, from IL-15-deficient mice.
120	16619285	The lectin-like stimulatory receptor natural killer group 2D (NKG2D) was up-regulated on CD8+ T cells only from wild-type mice, but not from IL-15-deficient mice.
121	16619285	Mechanistically, blocking NKG2D function with an mAb inhibited M. tuberculosis-directed CD8+ T cell responses in vitro.
122	16619285	We conclude that in addition to regulating the expansion of CD8+ T cells, IL-15 is also necessary for inducing effector mechanisms in CD8+ T cells that depend on NKG2D expression.
123	16619285	Hence, our results implicate IL-15 and NKG2D as promising targets for modulating CD8+ T cell-mediated protection against tuberculosis.
124	16754847	Nonetheless, tumor cell shedding of NKG2D ligands, such as MHC class I chain-related protein A (MICA), results in immune suppression through down-regulation of NKG2D surface expression.
125	16754847	Here we show that some patients who respond to antibody-blockade of cytotoxic T lymphocyte-associated antigen 4 or vaccination with lethally irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor generate high titer antibodies against MICA.
126	16754847	These humoral reactions are associated with a reduction of circulating soluble MICA (sMICA) and an augmentation of natural killer (NK) cell and CD8(+) T lymphocyte cytotoxicity.
127	16754847	Together, these findings establish a key role for the NKG2D pathway in the clinical activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade and granulocyte-macrophage colony-stimulating factor secreting tumor cell vaccines.
128	16754847	Nonetheless, tumor cell shedding of NKG2D ligands, such as MHC class I chain-related protein A (MICA), results in immune suppression through down-regulation of NKG2D surface expression.
129	16754847	Here we show that some patients who respond to antibody-blockade of cytotoxic T lymphocyte-associated antigen 4 or vaccination with lethally irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor generate high titer antibodies against MICA.
130	16754847	These humoral reactions are associated with a reduction of circulating soluble MICA (sMICA) and an augmentation of natural killer (NK) cell and CD8(+) T lymphocyte cytotoxicity.
131	16754847	Together, these findings establish a key role for the NKG2D pathway in the clinical activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade and granulocyte-macrophage colony-stimulating factor secreting tumor cell vaccines.
132	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
133	17462078	In this study we investigated CD94 and NKG2 gene expression in memory CD4 T-cell clones established from the spleens of C57BL/10 (H-2(b)) and BALB/c (H-2(d)) mice infected with influenza A virus (H3N2).
134	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
135	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
136	17462078	Despite CD94 being potentially an important marker for Th1 cells involved in virus infection, however, there has been little investigation of its expression or function in the CD4 T-cell lineage and no studies have looked at in-vivo-generated Th cells or memory cells.
137	17462078	We show in this study that in-vivo-generated CD4 Th1 cells, but not Th2 cells, exhibited full-length CD94 and NKG2A gene expression following activation with viral peptide.
138	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
139	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
140	17804754	This complex is chaperoned by heat shock protein Gp96, which mediates ISMMC uptake by antigen-presenting cells through the scavenger receptor CD91.
141	17804754	RNAs in ISMMC stimulate immature dendritic cells to secrete interleukin 12 and induce IFN-gamma in peripheral blood mononuclear cells.
142	17804754	On a total protein basis, Taxol induced ISMMC, expanded more CD8(+) cells, activated more CD56(+) NKG2D(+) cells to produce IFN-gamma, and were more potent inducers of high T-cell receptor density Perforin(+) cells than native ISMMC and peptide E75.
143	18202175	Here, we demonstrate that NKG2D, an activating receptor on natural killer (NK) cells, CD8(+) T lymphocytes, and MHC class I chain-related protein A (MICA), an NKG2D ligand induced in malignant plasma cells through DNA damage, contribute to the pathogenesis of MGUS and MM.
144	18202175	MICA expression is increased on plasma cells from MGUS patients compared with normal donors, whereas MM patients display intermediate MICA levels and a high expression of ERp5, a protein disulfide isomerase linked to MICA shedding (sMICA).
145	18364009	Enhancing the clinical activity of granulocyte-macrophage colony-stimulating factor-secreting tumor cell vaccines.
146	18364009	A comparative analysis of vaccination with irradiated, murine tumor cells engineered to express a large number of immunostimulatory molecules established the superior ability of granulocyte-macrophage colony-stimulating factor (GM-CSF) to evoke potent, specific, and long-lasting anti-tumor immunity.
147	18364009	These include milk fat globule epidermal growth factor protein-8 expansion of forkhead box protein 3+ regulatory T cells, cytotoxic T-lymphocyte antigen-4-mediated negative costimulation, and soluble major histocompatibility complex class I chain-related protein A suppression of NKG2D-dependent innate and adaptive anti-tumor cytotoxicity.
148	19319200	Dendritic cell-derived exosomes promote natural killer cell activation and proliferation: a role for NKG2D ligands and IL-15Ralpha.
149	19319200	Indeed, Dex promoted an IL-15Ralpha- and NKG2D-dependent NK cell proliferation and activation respectively, resulting in anti-metastatic effects mediated by NK1.1(+) cells.
150	19319200	In humans, Dex express functional IL-15Ralpha which allow proliferation and IFNgamma secretion by NK cells.
151	19319200	Dendritic cell-derived exosomes promote natural killer cell activation and proliferation: a role for NKG2D ligands and IL-15Ralpha.
152	19319200	Indeed, Dex promoted an IL-15Ralpha- and NKG2D-dependent NK cell proliferation and activation respectively, resulting in anti-metastatic effects mediated by NK1.1(+) cells.
153	19319200	In humans, Dex express functional IL-15Ralpha which allow proliferation and IFNgamma secretion by NK cells.
154	19769739	Through this approach, we uncovered the immunogenicity of major histocompatibility chain-related protein A (MICA), which is a ligand for NKG2D, and ERp5, a protein disulfide isomerase involved in MICA shedding.
155	19828769	Peripheral blood mononuclear cells isolated from infected animals are not productively infected, but virus exposure in vivo resulted in the significant induction of NKp30 and Toll-like receptor 3 expression and the moderate activation of SOCS3 and interleukin-15 receptor mRNA.
156	19828769	However, there was little alteration of mRNA expression from a number of other receptor genes in these cells, including SH2D1B and NKG2A (inhibitory) as well as NKp80, NKp46, and NKG2D (activating).
157	21122940	DAP10 contributes to CD8(+) T cell-mediated cytotoxic effector mechanisms during Mycobacterium tuberculosis infection.
158	21122940	The activating C-type lectin-like receptor NKG2D, which is expressed by mouse NK cells and activated CD8 T cells, was previously demonstrated to be involved in tumor rejection and as a defense mechanism against viral and bacterial infections.
159	21122940	Because CD8 T cells are important for protective immune responses during chronic Mycobacterium tuberculosis (Mtb) infection and represent a promising target for new vaccine strategies to prevent human pulmonary tuberculosis (TB), we studied the immune response in mice deficient for the NKG2D adapter molecule DAP10 during experimental TB.
160	21122940	After aerosol infection, DAP10-defcient mice displayed an unimpaired recruitment, activation and development of antigen-specific CD8 T cells.
161	21122940	Whereas the frequency of interferon-gamma-producing CD8 T cells from Mtb-infected DAP10-defcient mice was not affected, CD8 T cell-mediated cytotoxicity was significantly reduced in the absence of DAP10.
162	21122940	The loss of cytotoxic activity in DAP10-deficient CD8 T cells was associated with an impaired release of cytotoxic granules.
163	21122940	Together, our results suggest that during Mtb infection DAP10 is required for maximal cytolytic activity of CD8 T cells.
164	21122940	DAP10 contributes to CD8(+) T cell-mediated cytotoxic effector mechanisms during Mycobacterium tuberculosis infection.
165	21122940	The activating C-type lectin-like receptor NKG2D, which is expressed by mouse NK cells and activated CD8 T cells, was previously demonstrated to be involved in tumor rejection and as a defense mechanism against viral and bacterial infections.
166	21122940	Because CD8 T cells are important for protective immune responses during chronic Mycobacterium tuberculosis (Mtb) infection and represent a promising target for new vaccine strategies to prevent human pulmonary tuberculosis (TB), we studied the immune response in mice deficient for the NKG2D adapter molecule DAP10 during experimental TB.
167	21122940	After aerosol infection, DAP10-defcient mice displayed an unimpaired recruitment, activation and development of antigen-specific CD8 T cells.
168	21122940	Whereas the frequency of interferon-gamma-producing CD8 T cells from Mtb-infected DAP10-defcient mice was not affected, CD8 T cell-mediated cytotoxicity was significantly reduced in the absence of DAP10.
169	21122940	The loss of cytotoxic activity in DAP10-deficient CD8 T cells was associated with an impaired release of cytotoxic granules.
170	21122940	Together, our results suggest that during Mtb infection DAP10 is required for maximal cytolytic activity of CD8 T cells.
171	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
172	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
173	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
174	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
175	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
176	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
177	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
178	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
179	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
180	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
181	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
182	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
183	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
184	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
185	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
186	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
187	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
188	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
189	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
190	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
191	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
192	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
193	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
194	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
195	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
196	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
197	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
198	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
199	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
200	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
201	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
202	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
203	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
204	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
205	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
206	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
207	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
208	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
209	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
210	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
211	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
212	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
213	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
214	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
215	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
216	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
217	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
218	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
219	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
220	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
221	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
222	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
223	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
224	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
225	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
226	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
227	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
228	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
229	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
230	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
231	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
232	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
233	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
234	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
235	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
236	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
237	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
238	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
239	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
240	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
241	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
242	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
243	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
244	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
245	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
246	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
247	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
248	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
249	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
250	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
251	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
252	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
253	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
254	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
255	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
256	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
257	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
258	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
259	21210234	NKG2D expression in CD4+ T lymphocytes as a marker of senescence in the aged immune system.
260	21210234	These changes are more frequently found in CD8+ T cells, and there are not well-defined markers of differentiation in the CD4+ subset.
261	21210234	Typical features of cell immunosenescence are characteristics of pathologies in which the aberrant expression of NKG2D in CD4+ T cells has been described.
262	21210234	To evaluate a possible age-related expression of NKG2D in CD4+ T cells, we compared their percentage in peripheral blood from 100 elderly and 50 young adults.
263	21210234	The median percentage of CD4+ NKG2D+ in elders was 5.3% (interquartile range (IR): 8.74%) versus 1.4% (IR: 1.7%) in young subjects (p < 0.3 × 10(-10)).
264	21210234	CD28 expression distinguished two subsets of CD4+ NKG2D+ cells with distinct functional properties and differentiation status.
265	21210234	CD28+ cells showed an immature phenotype associated with high frequencies of CD45RA and CD31.
266	21210234	However, most of the NKG2D+ cells belonged to the CD28(null) compartment and shared their phenotypical properties.
267	21210234	Moreover, the frequency of the CD4+ NKG2D+ subset was clearly related to the status of the T cells.
268	21210234	Higher frequencies of the NKG2D+ subset were accompanied with a gradual decrease of NAIVE and central memory cells, but also with a higher level of more differentiated subsets of CD4+ T cells.
269	21210234	In conclusion, CD4+ NKG2D+ represent a subset of highly differentiated T cells which characterizes the senescence of the immune system.
270	21422297	Subsets of T cells could be defined based on their expression of Eomes, Cxcr3, and Ccr7, or Klrk1, Klrg1, and Ccr5 in CM and EM cells, respectively.
271	21422297	Of EM cells elicited by DNA-rAd, 74% were Klrk1(-) Klrg1(-)Ccr5(-) compared with only 26% and 20% for rAd5-rAd5 or rAd5-LCMV.
272	21422297	Subsets of T cells could be defined based on their expression of Eomes, Cxcr3, and Ccr7, or Klrk1, Klrg1, and Ccr5 in CM and EM cells, respectively.
273	21422297	Of EM cells elicited by DNA-rAd, 74% were Klrk1(-) Klrg1(-)Ccr5(-) compared with only 26% and 20% for rAd5-rAd5 or rAd5-LCMV.
274	22484802	This review also disproves our contemporary understanding of the versatile regulators of DNA damage repair (ATM, ATR) that trigger cell surface expression of NKG2D ligands and consequent elimination of the tumor cells by NK cells and other lymphocytes that express NK cell receptors.
275	22509395	Tumor-targeted delivery of IL-2 by NKG2D leads to accumulation of antigen-specific CD8+ T cells in the tumor loci and enhanced anti-tumor effects.
276	22509395	Because NKG2D ligands have been shown to be highly expressed in many cancer cells but not in healthy cells, we reason that a chimeric protein consisting of NKG2D linked to IL-2 will lead to the specific targeting of IL-2 to the tumor location.
277	22509395	Therefore, we created chimeric proteins consisting of NKG2D linked to Gaussia luciferase (GLuc; a marker protein) or IL-2 to form NKG2D-Fc-GLuc and NKG2D-Fc-IL2, respectively.
278	22509395	Furthermore, we showed that TC-1 tumor-bearing mice intramuscularly injected with DNA encoding NKG2D-Fc-IL2, followed by electroporation, exhibited an increased number of luciferase-expressing E7-specific CD8+ T cells at the tumor location.
279	22509395	Therefore, by linking NKG2D to IL2, we are able to specifically deliver IL-2 to the tumor location, enhancing antigen-specific T-cell immune response and controlling tumor growth.
280	22509395	Tumor-targeted delivery of IL-2 by NKG2D leads to accumulation of antigen-specific CD8+ T cells in the tumor loci and enhanced anti-tumor effects.
281	22509395	Because NKG2D ligands have been shown to be highly expressed in many cancer cells but not in healthy cells, we reason that a chimeric protein consisting of NKG2D linked to IL-2 will lead to the specific targeting of IL-2 to the tumor location.
282	22509395	Therefore, we created chimeric proteins consisting of NKG2D linked to Gaussia luciferase (GLuc; a marker protein) or IL-2 to form NKG2D-Fc-GLuc and NKG2D-Fc-IL2, respectively.
283	22509395	Furthermore, we showed that TC-1 tumor-bearing mice intramuscularly injected with DNA encoding NKG2D-Fc-IL2, followed by electroporation, exhibited an increased number of luciferase-expressing E7-specific CD8+ T cells at the tumor location.
284	22509395	Therefore, by linking NKG2D to IL2, we are able to specifically deliver IL-2 to the tumor location, enhancing antigen-specific T-cell immune response and controlling tumor growth.
285	22509395	Tumor-targeted delivery of IL-2 by NKG2D leads to accumulation of antigen-specific CD8+ T cells in the tumor loci and enhanced anti-tumor effects.
286	22509395	Because NKG2D ligands have been shown to be highly expressed in many cancer cells but not in healthy cells, we reason that a chimeric protein consisting of NKG2D linked to IL-2 will lead to the specific targeting of IL-2 to the tumor location.
287	22509395	Therefore, we created chimeric proteins consisting of NKG2D linked to Gaussia luciferase (GLuc; a marker protein) or IL-2 to form NKG2D-Fc-GLuc and NKG2D-Fc-IL2, respectively.
288	22509395	Furthermore, we showed that TC-1 tumor-bearing mice intramuscularly injected with DNA encoding NKG2D-Fc-IL2, followed by electroporation, exhibited an increased number of luciferase-expressing E7-specific CD8+ T cells at the tumor location.
289	22509395	Therefore, by linking NKG2D to IL2, we are able to specifically deliver IL-2 to the tumor location, enhancing antigen-specific T-cell immune response and controlling tumor growth.
290	22509395	Tumor-targeted delivery of IL-2 by NKG2D leads to accumulation of antigen-specific CD8+ T cells in the tumor loci and enhanced anti-tumor effects.
291	22509395	Because NKG2D ligands have been shown to be highly expressed in many cancer cells but not in healthy cells, we reason that a chimeric protein consisting of NKG2D linked to IL-2 will lead to the specific targeting of IL-2 to the tumor location.
292	22509395	Therefore, we created chimeric proteins consisting of NKG2D linked to Gaussia luciferase (GLuc; a marker protein) or IL-2 to form NKG2D-Fc-GLuc and NKG2D-Fc-IL2, respectively.
293	22509395	Furthermore, we showed that TC-1 tumor-bearing mice intramuscularly injected with DNA encoding NKG2D-Fc-IL2, followed by electroporation, exhibited an increased number of luciferase-expressing E7-specific CD8+ T cells at the tumor location.
294	22509395	Therefore, by linking NKG2D to IL2, we are able to specifically deliver IL-2 to the tumor location, enhancing antigen-specific T-cell immune response and controlling tumor growth.
295	22509395	Tumor-targeted delivery of IL-2 by NKG2D leads to accumulation of antigen-specific CD8+ T cells in the tumor loci and enhanced anti-tumor effects.
296	22509395	Because NKG2D ligands have been shown to be highly expressed in many cancer cells but not in healthy cells, we reason that a chimeric protein consisting of NKG2D linked to IL-2 will lead to the specific targeting of IL-2 to the tumor location.
297	22509395	Therefore, we created chimeric proteins consisting of NKG2D linked to Gaussia luciferase (GLuc; a marker protein) or IL-2 to form NKG2D-Fc-GLuc and NKG2D-Fc-IL2, respectively.
298	22509395	Furthermore, we showed that TC-1 tumor-bearing mice intramuscularly injected with DNA encoding NKG2D-Fc-IL2, followed by electroporation, exhibited an increased number of luciferase-expressing E7-specific CD8+ T cells at the tumor location.
299	22509395	Therefore, by linking NKG2D to IL2, we are able to specifically deliver IL-2 to the tumor location, enhancing antigen-specific T-cell immune response and controlling tumor growth.
300	22573736	We found a significant increase in the expression of ILT2 by NK and CD3(+) CD56(+) lymphocytes and monocytes after quadrivalent HPV (type 6/11/16/18) vaccine immunization.
301	22573736	In addition, the in vitro stimulation with the quadrivalent HPV (type 6/11/16/18) vaccine also increased the proportion of CD3(-) CD56(+) ILT2(+) NK cells.
302	22573736	Finally, a significant increase in the expression of NKG2D, NKp30, and NKp46 by NK and CD3(+) CD56(+) lymphocytes was detected after quadrivalent HPV (type 6/11/16/18) vaccine immunization.
303	22641658	Cancer immunotherapy using NKG2D and DNAM-1 systems.
304	22641658	NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells.
305	22641658	Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting.
306	22641658	Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia.
307	22641658	Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
308	22641658	Cancer immunotherapy using NKG2D and DNAM-1 systems.
309	22641658	NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells.
310	22641658	Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting.
311	22641658	Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia.
312	22641658	Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
313	22641658	Cancer immunotherapy using NKG2D and DNAM-1 systems.
314	22641658	NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells.
315	22641658	Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting.
316	22641658	Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia.
317	22641658	Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
318	22641658	Cancer immunotherapy using NKG2D and DNAM-1 systems.
319	22641658	NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells.
320	22641658	Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting.
321	22641658	Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia.
322	22641658	Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
323	22641658	Cancer immunotherapy using NKG2D and DNAM-1 systems.
324	22641658	NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells.
325	22641658	Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting.
326	22641658	Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia.
327	22641658	Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
328	22977597	The results indicated that the B16F10 tumor cell vaccine treated with MIT alone or in combination with reserpine (RP) and verapamil (VP) for 12 h triggered apoptosis, and that the expression of CD80, the MHC II class molecule, NKG2D and its ligand were significantly increased compared to the expression levels in the control group.
329	23523350	Bystander-activated memory CD8 T cells control early pathogen load in an innate-like, NKG2D-dependent manner.
330	24052528	NKG2D is one of the most important activating NK cell receptors that plays a role in costimulation of CD8 T cells.
331	24052528	Here we demonstrate that the expression of CD8 T-cell epitope of Listeria monocytogenes by a recombinant mouse CMV (MCMV) expressing the NKG2D ligand retinoic acid early-inducible protein 1-gamma (RAE-1γ) dramatically enhanced the effectiveness and longevity of epitope-specific CD8 T-cell response and conferred protection against a subsequent challenge infection with Listeria monocytogenes.
332	24052528	Unexpectedly, the attenuated growth in vivo of the CMV vector expressing RAE-1γ and its capacity to enhance specific CD8 T-cell response were preserved even in mice lacking NKG2D, implying additional immune function for RAE-1γ beyond engagement of NKG2D.
333	24052528	NKG2D is one of the most important activating NK cell receptors that plays a role in costimulation of CD8 T cells.
334	24052528	Here we demonstrate that the expression of CD8 T-cell epitope of Listeria monocytogenes by a recombinant mouse CMV (MCMV) expressing the NKG2D ligand retinoic acid early-inducible protein 1-gamma (RAE-1γ) dramatically enhanced the effectiveness and longevity of epitope-specific CD8 T-cell response and conferred protection against a subsequent challenge infection with Listeria monocytogenes.
335	24052528	Unexpectedly, the attenuated growth in vivo of the CMV vector expressing RAE-1γ and its capacity to enhance specific CD8 T-cell response were preserved even in mice lacking NKG2D, implying additional immune function for RAE-1γ beyond engagement of NKG2D.
336	24052528	NKG2D is one of the most important activating NK cell receptors that plays a role in costimulation of CD8 T cells.
337	24052528	Here we demonstrate that the expression of CD8 T-cell epitope of Listeria monocytogenes by a recombinant mouse CMV (MCMV) expressing the NKG2D ligand retinoic acid early-inducible protein 1-gamma (RAE-1γ) dramatically enhanced the effectiveness and longevity of epitope-specific CD8 T-cell response and conferred protection against a subsequent challenge infection with Listeria monocytogenes.
338	24052528	Unexpectedly, the attenuated growth in vivo of the CMV vector expressing RAE-1γ and its capacity to enhance specific CD8 T-cell response were preserved even in mice lacking NKG2D, implying additional immune function for RAE-1γ beyond engagement of NKG2D.
339	24590060	RAE1 ligands for the NKG2D receptor are regulated by STING-dependent DNA sensor pathways in lymphoma.
340	24590060	Here, we report that the induction of retinoic acid early transcript 1 (RAE1) ligands for NKG2D by the DDR relies on a STING-dependent DNA sensor pathway involving the effector molecules TBK1 and IRF3.
341	24590060	RAE1 ligands for the NKG2D receptor are regulated by STING-dependent DNA sensor pathways in lymphoma.
342	24590060	Here, we report that the induction of retinoic acid early transcript 1 (RAE1) ligands for NKG2D by the DDR relies on a STING-dependent DNA sensor pathway involving the effector molecules TBK1 and IRF3.
343	24777763	NK cells are primed by ANRS MVA(HIV)-infected DCs, via a mechanism involving NKG2D and membrane-bound IL-15, to control HIV-1 infection in CD4+ T cells.
344	24777763	We also highlight the importance of NKG2D engagement on NK cells and DC-produced IL-15 to achieve the anti-HIV-1 specific priming, as blockade of either NKG2D or IL-15 during MVA(HIV)-priming lead to a subsequent decreased control of HIV-1 infection in autologous CD4(+) T cells.
345	24777763	Furthermore, we show that the decreased control of HIV-1 infection in CD4(+) T cells might be due, at least in part, to the decreased expression of membrane-bound IL-15 (mbIL-15) on DCs when NKG2D is blocked during MVA(HIV)-priming of NK cells.
346	24777763	NK cells are primed by ANRS MVA(HIV)-infected DCs, via a mechanism involving NKG2D and membrane-bound IL-15, to control HIV-1 infection in CD4+ T cells.
347	24777763	We also highlight the importance of NKG2D engagement on NK cells and DC-produced IL-15 to achieve the anti-HIV-1 specific priming, as blockade of either NKG2D or IL-15 during MVA(HIV)-priming lead to a subsequent decreased control of HIV-1 infection in autologous CD4(+) T cells.
348	24777763	Furthermore, we show that the decreased control of HIV-1 infection in CD4(+) T cells might be due, at least in part, to the decreased expression of membrane-bound IL-15 (mbIL-15) on DCs when NKG2D is blocked during MVA(HIV)-priming of NK cells.
349	24777763	NK cells are primed by ANRS MVA(HIV)-infected DCs, via a mechanism involving NKG2D and membrane-bound IL-15, to control HIV-1 infection in CD4+ T cells.
350	24777763	We also highlight the importance of NKG2D engagement on NK cells and DC-produced IL-15 to achieve the anti-HIV-1 specific priming, as blockade of either NKG2D or IL-15 during MVA(HIV)-priming lead to a subsequent decreased control of HIV-1 infection in autologous CD4(+) T cells.
351	24777763	Furthermore, we show that the decreased control of HIV-1 infection in CD4(+) T cells might be due, at least in part, to the decreased expression of membrane-bound IL-15 (mbIL-15) on DCs when NKG2D is blocked during MVA(HIV)-priming of NK cells.
352	25131736	Furthermore, we observed that NK cell receptors NKG2D and NKp46 modulate the priming of NK cells.
353	25229656	NK cells in the presence of HPV-VLPs enhanced DC-maturation as shown by an upregulation of CD86 and HLA-DR and an increased production of IL-12p70, but not of the immunosuppressive cytokine IL-10.
354	25229656	This crosstalk between NK cells and DCs needed CD40 interaction and IL-12p70 secretion, whereas NKG2D was not implicated.
355	26022121	The fused dsNKG2D-IL-15 gene fragment consisted of double extracellular domains of NKG2D with IL-15 gene at downstream.
356	26284472	NKG2D ligands (NKG2DLs) are a group of stress-inducible major histocompatibility complex (MHC) class I-like molecules that act as a danger signal alerting the immune system to the presence of abnormal cells.
357	26284472	Some mammals have a third family of NKG2DL-like class I genes which we named MILL (MHC class I-like located near the leukocyte receptor complex).