Ignet

Gene Information

Gene symbol: KLRC1

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

HGNC ID: 6374

Synonyms: NKG2-A, NKG2-B, CD159a

Related Genes

#	Gene Symbol	Number of hits
1	ABL2	1 hits
2	CD4	1 hits
3	CD8A	1 hits
4	FCGR3A	1 hits
5	HLA-A	1 hits
6	HLA-E	1 hits
7	ICT1	1 hits
8	IL15	1 hits
9	IL17A	1 hits
10	IL7	1 hits
11	KIR2DL1	1 hits
12	KIR3DL1	1 hits
13	KLRB1	1 hits
14	KLRD1	1 hits
15	KLRG1	1 hits
16	KLRK1	1 hits
17	NCR1	1 hits
18	NCR2	1 hits
19	P4HB	1 hits
20	SH2D1B	1 hits

Related Sentences

#	PMID	Sentence
1	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
2	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
3	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
4	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
5	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
6	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
7	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
8	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
9	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
10	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
11	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
12	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
13	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
14	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
15	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
16	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
17	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
18	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
19	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
20	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
21	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
22	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
23	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
24	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
25	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
26	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
27	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
28	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
29	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
30	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
31	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
32	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
33	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
34	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
35	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
36	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
37	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
38	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
39	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
40	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
41	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
42	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
43	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
44	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
45	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
46	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
47	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
48	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
49	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
50	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
51	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
52	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
53	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
54	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
55	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
56	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
57	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
58	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
59	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
60	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
61	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
62	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
63	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
64	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
65	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
66	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
67	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
68	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
69	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
70	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
71	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
72	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
73	12097371	CD94/NKG2 expression does not inhibit cytotoxic function of lymphocytic choriomeningitis virus-specific CD8+ T cells.
74	12097371	Following acute infection of C57BL/6 and BALB/cJ mice with lymphocytic choriomeningitis virus (LCMV), we observed that Ag-specific CD8(+) T cells expressed CD94/NKG2.
75	12097371	Expression of CD94/NKG2 was maintained for at least 1 year following LCMV infection, as was the NKT cell marker.
76	12097371	By means of cell sorting and quantitative PCR, we found that NP118-specific CD8(+) T cells primarily express transcripts for inhibitory NKG2 receptor isoforms.
77	12097371	CD94/NKG2 expression was also observed on Ag-specific CD8(+) T cells following infection with polyoma virus, influenza virus, and Listeria monocytogenes, suggesting that it may be a common characteristic of Ag-specific CD8(+) T cells following infection with viral or bacterial pathogens.
78	12097371	Expression of CD94/NKG2 on memory-specific CD8(+) T cells did not change following secondary challenge with LCMV clone 13 and did not inhibit viral clearance.
79	12097371	Furthermore, we found no evidence that CD94/NKG2 inhibits either the lytic function of LCMV-specific T cells or their capacity to produce effector cytokines upon peptide stimulation.
80	12097371	Finally, down-regulation of CD94/NKG2 was found to occur only during chronic LCMV infection.
81	12097371	Altogether, this study suggests that CD94/NKG2 expression is not necessarily correlated with inhibition of T cell function.
82	12874227	Analysis of HLA-E peptide-binding specificity and contact residues in bound peptide required for recognition by CD94/NKG2.
83	12874227	The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule.
84	12874227	Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors.
85	12874227	A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2.
86	12874227	Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.
87	12874227	Analysis of HLA-E peptide-binding specificity and contact residues in bound peptide required for recognition by CD94/NKG2.
88	12874227	The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule.
89	12874227	Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors.
90	12874227	A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2.
91	12874227	Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.
92	12874227	Analysis of HLA-E peptide-binding specificity and contact residues in bound peptide required for recognition by CD94/NKG2.
93	12874227	The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule.
94	12874227	Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors.
95	12874227	A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2.
96	12874227	Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.
97	12874227	Analysis of HLA-E peptide-binding specificity and contact residues in bound peptide required for recognition by CD94/NKG2.
98	12874227	The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule.
99	12874227	Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors.
100	12874227	A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2.
101	12874227	Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.
102	12874227	Analysis of HLA-E peptide-binding specificity and contact residues in bound peptide required for recognition by CD94/NKG2.
103	12874227	The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule.
104	12874227	Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors.
105	12874227	A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2.
106	12874227	Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.
107	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
108	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).
109	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
110	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
111	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.
112	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.
113	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
114	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
115	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
116	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).
117	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
118	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
119	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.
120	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.
121	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
122	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
123	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
124	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).
125	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
126	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
127	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.
128	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.
129	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
130	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
131	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
132	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).
133	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
134	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
135	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.
136	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.
137	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
138	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
139	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
140	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).
141	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
142	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
143	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.
144	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.
145	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
146	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
147	17462078	Differential induction of CD94 and NKG2 in CD4 helper T cells.
148	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).
149	17462078	CD94 and NKG2A/C/E proteins form heterodimeric membrane receptors that are involved in virus recognition.
150	17462078	CD94 and NKG2 expression have been well characterized in natural killer (NK) and cytotoxic T cells.
151	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.
152	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.
153	17462078	Another member of the NK receptor family, NKG2D, but not NKG2C or E, was also differentially expressed in Th1 cells.
154	17462078	We show here that CD94 and NKG2A may exist as multiple isoforms with the potential to distinguish helper T-cell subsets.
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	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
158	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
159	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
160	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
161	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
162	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
163	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
164	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
165	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
166	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
167	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
168	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
169	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
170	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
171	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
172	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
173	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
174	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
175	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
176	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
177	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
178	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
179	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
180	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
181	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
182	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
183	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
184	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
185	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
186	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
187	21346231	KLRG1+NKG2A+ CD8 T cells mediate protection and participate in memory responses during γ-herpesvirus infection.
188	21346231	During γHV68 persistence, ∼75% of γHV68-specific CD8 T cells coexpress the NK receptors killer cell lectin-like receptor G1 (KLRG1) and NKG2A.
189	21346231	In this study, we take advantage of this unique phenotype to analyze the capacity of CD8 T cells expressing or not expressing KLRG1 and NKG2A to mediate effector and memory responses.
190	21346231	Our results show that γHV68-specific KLRG1(+)NKG2A(+) CD8 T cells have an effector memory phenotype as well as characteristics of polyfunctional effector cells such us IFN-γ and TNF-α production, killing capacity, and are more efficient at protecting against a γHV68 challenge than their NKG2A(-)KLRG1(-) counterparts.
191	21346231	Nevertheless, γHV68-specific NKG2A(+)KLRG1(+) CD8 T cells express IL-7 and IL-15 receptors, can survive long-term without cognate Ag, and subsequently mount a protective response during antigenic recall.
192	21346231	These results highlight the plasticity of the immune system to generate protective effector and proliferative memory responses during virus persistence from a pool of KLRG1(+)NKG2A(+) effector memory CD8 T cells.
193	23620737	Comprehensive studies of the frequencies and absolute numbers of the various cell lineages that synthesize IL-17 in the blood and corresponding gastrointestinal (GI) tissues, their correlation with CD4(+) Tregs, CD8(+) Tregs, total and IFN-α synthesizing plasmacytoid dendritic cells (pDC) relative to plasma viral load in SIV infection has been lacking.
194	23620737	Highlights of the differences between EC and HVL RM within Gastro-intestinal tissues (GIT) was the maintenance and/or increases in the levels of IL-17 synthesizing CD4, CD8, and NK cells and pDCs associated with slight decreases in the levels of CD4(+) Tregs and IFN-α synthesizing pDCs in EC as compared with decreases in the levels of IL-17 synthesizing CD4, CD8 and NK cells associated with increases in pDCs and IFN-α synthesizing pDCs in HVL monkeys.
195	23620737	Positive correlations between plasma VL and decreases in the levels of Th17, Tc17, NK-17, CD4(+) Tregs and increases in the levels of CD8(+) Tregs, total and IFN-α synthesizing pDCs were also noted.
196	23620737	This study also identified 2 additional IL-17(+) subsets in GIT as CD3(-/)CD8(+)/NKG2a(-) and CD3(+)/CD8(+)/NKG2a(+) subsets.
197	23784853	We decided to assess the levels of NK and NKT lymphocytes and the expression levels of different membrane receptors (NKp44, NKp46, NKG2A, killer cell immune-like receptor [KIR] 3DL1/DS1, KIR2DL1/DS1, and CD161) in peripheral blood samples of patients with influenza (n = 17) and healthy individuals immunized against this virus (seasonal and [H1N1]pdm2009 influenza vaccines; n = 15 and 12, respectively).
198	23784853	We found that the patients with severe influenza (n = 9) showed significant increases in the percentages of NKp46(+) NKp44(+) NK cells and the proportions of NK and NKT lymphocytes expressing KIR2DL1 and KIR3DL1 and reductions in the percentages of NKp46(+) NKp44(-) NK cells compared to those in the healthy controls (n = 27).
199	24503100	During SIV infection, blood CD16 and mucosal NKG2A(+) subsets had increased cytotoxic potential.
200	24503100	Antiretroviral therapy significantly increased the frequency of mucosal NKG2A(+) NK cells and peripheral CD16(+) NK cells.
201	24503100	During SIV infection, blood CD16 and mucosal NKG2A(+) subsets had increased cytotoxic potential.
202	24503100	Antiretroviral therapy significantly increased the frequency of mucosal NKG2A(+) NK cells and peripheral CD16(+) NK cells.
203	26453750	Human cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A were transfected with IL-15Rα.
204	26453750	Proliferation of primary NK cells in response to transpresented IL-15 was reduced by engagement of either KIR2DL1 or KIR2DL2/3 by cognate HLA-C ligands.
205	26453750	Inhibitory KIR-HLA-C interactions did not reduce the proliferation induced by soluble IL-15.
206	26453750	Therefore, transpresentation of IL-15 is subject to downregulation by MHC class I-specific inhibitory receptors.
207	26453750	Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E.
208	26453750	Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein.