Ignet

Gene Information

Gene symbol: CD1D

Gene name: CD1d molecule

HGNC ID: 1637

Related Genes

#	Gene Symbol	Number of hits
1	APC	1 hits
2	CCR5	1 hits
3	CD160	1 hits
4	CD1A	1 hits
5	CD4	1 hits
6	CD8A	1 hits
7	COL1A1	1 hits
8	HLA-A	1 hits
9	IDDM2	1 hits
10	IFNA1	1 hits
11	IFNG	1 hits
12	IL10	1 hits
13	IL12A	1 hits
14	IL2	1 hits
15	IL2RA	1 hits
16	IL4	1 hits
17	IL6	1 hits
18	INS	1 hits
19	KIR2DS2	1 hits
20	KLRB1	1 hits
21	MAPK3	1 hits
22	MICB	1 hits
23	MR1	1 hits
24	NFKB1	1 hits
25	PSIP1	1 hits
26	TNF	1 hits
27	TRA	1 hits
28	TRB	1 hits
29	UGCG	1 hits

Related Sentences

#	PMID	Sentence
1	10707937	Sections from the pancreata of these injected mice were stained for cytokines (tumor necrosis factor alpha [TNF-alpha], interferon gamma [IFN-gamma], CD1d, interleukin 2 [IL-2], IL-4, IL-6, IL-10, and IL-12).
2	10707937	The expression of IL-2 and IL-12 was very scarce.
3	10839805	In contrast, natural killer (NK) cells failed to bind the tetramers either empty or loaded with alphaGalCer, suggesting the absence of a CD1d-specific, antigen-nonspecific NK receptor.
4	11358978	A subset of CD161 (NK1) T cells express an invariant Valpha14Jalpha281 TCR-alpha chain (Valpha(invt) T cells) and produce Th2 and Th1 cytokines rapidly in response to CD1d, but their physiological function(s) remain unclear.
5	11907079	First, they are restricted by a nonclassical MHC class I molecule, CD1d, which presents glycolipids; second, their TCR repertoire is very limited.
6	11907079	After stimulation by their TCR, NKT cells rapidly release large amounts of cytokines, such as IL-4 and IFN-gamma.
7	11907079	Analysis of cytokine production by NKT cells from splanchnic lymph nodes reveals that they produce at least as much IL-4 as IFN-gamma, in contrast to NKT cells from other organs (spleen, liver, and peripheral lymph nodes), which produce much more IFN-gamma than IL-4.
8	12144618	NKT cells represent a unique T cell lineage that recognize glycolipid antigens in the context of the non-classical MHC class I molecule CD1d.
9	12235110	Defects in IL-4-producing CD1d-autoreactive NKT cells have been implicated in numerous Th1-mediated autoimmune diseases, including diabetes, multiple sclerosis, rheumatoid arthritis, lupus, and systemic sclerosis.
10	12235110	Particular attention has been focused on autoimmune insulin-dependent diabetes mellitus (IDDM) because nonobese diabetic (NOD) mice and humans with IDDM are both reported to express severe deficiencies in the frequency and Th2 functions of NKT cells.
11	12235110	We have now devised a direct, highly specific CD1d tetramer-based methodology to test whether humans with IDDM have associated NKT cell defects.
12	12235110	Surprisingly, although we find marked and stable differences in NKT cells between individuals, our study of IDDM patients and healthy controls, including discordant twin pairs, demonstrates that NKT cell frequency and IL-4 production are conserved during the course of IDDM.
13	12235110	Defects in IL-4-producing CD1d-autoreactive NKT cells have been implicated in numerous Th1-mediated autoimmune diseases, including diabetes, multiple sclerosis, rheumatoid arthritis, lupus, and systemic sclerosis.
14	12235110	Particular attention has been focused on autoimmune insulin-dependent diabetes mellitus (IDDM) because nonobese diabetic (NOD) mice and humans with IDDM are both reported to express severe deficiencies in the frequency and Th2 functions of NKT cells.
15	12235110	We have now devised a direct, highly specific CD1d tetramer-based methodology to test whether humans with IDDM have associated NKT cell defects.
16	12235110	Surprisingly, although we find marked and stable differences in NKT cells between individuals, our study of IDDM patients and healthy controls, including discordant twin pairs, demonstrates that NKT cell frequency and IL-4 production are conserved during the course of IDDM.
17	14561706	The CD1d-reactive tetramer-positive CD4+ T cells augmented anti-dsDNA Ab secretion about tenfold.
18	14632651	CD1d-reactive natural killer T (NKT) cells can rapidly produce T helper type 1 (Th1) and/or Th2 cytokines, can activate antigen-presenting cell (APC) interleukin-12 (IL-12) production, and are implicated in the regulation of adaptive immune responses.
19	14632651	EMCV-D resistance depends on IL-12-mediated interferon-gamma (IFN-gamma) production.
20	14632651	We propose that CD1d-reactive T cells respond to early immune signals and function in the innate immune response to a physiological viral infection by rapidly augmenting APC IL-12 production and activating NK cells.
21	14632651	CD1d-reactive natural killer T (NKT) cells can rapidly produce T helper type 1 (Th1) and/or Th2 cytokines, can activate antigen-presenting cell (APC) interleukin-12 (IL-12) production, and are implicated in the regulation of adaptive immune responses.
22	14632651	EMCV-D resistance depends on IL-12-mediated interferon-gamma (IFN-gamma) production.
23	14632651	We propose that CD1d-reactive T cells respond to early immune signals and function in the innate immune response to a physiological viral infection by rapidly augmenting APC IL-12 production and activating NK cells.
24	15111500	Interleukin-4 but not interleukin-10 protects against spontaneous and recurrent type 1 diabetes by activated CD1d-restricted invariant natural killer T-cells.
25	15111500	Although interleukin (IL)-4 and IL-10 have been implicated in alpha-GalCer-induced protection from type 1 diabetes, a precise role for these cytokines in iNKT cell regulation of susceptibility to type 1 diabetes has not been identified.
26	15111500	Here we use NOD.IL-4(-/-) and NOD.IL-10(-/-) knockout mice to further evaluate the roles of IL-4 and IL-10 in alpha-GalCer-induced protection from type 1 diabetes.
27	15111500	We found that IL-4 but not IL-10 expression mediates protection against spontaneous type 1 diabetes, recurrent type 1 diabetes, and prolonged syngeneic islet graft function.
28	15111500	Increased transforming growth factor-beta gene expression in pancreatic lymph nodes may be involved in alpha-GalCer-mediated protection in NOD.IL-10(-/-) knockout mice.
29	15111500	Unlike the requirement of IL-7 and IL-15 to maintain iNKT cell homeostasis, IL-4 and IL-10 are not required for alpha-GalCer-induced iNKT cell expansion and/or survival.
30	15128771	To test this hypothesis, we transgenically overexpressed CD1d molecules under the control of the insulin promoter within the pancreatic islets of NOD mice (insCD1d).
31	15322171	We now show that overexpression in NOD mice of CD1d-restricted TCR Valpha3.2(+)Vbeta9(+) NKT cells producing high levels of IFN-gamma but low amounts of IL-4 leads to prevention of type 1 diabetes, demonstrating a role for nonclassical CD1d-restricted NKT cells in the regulation of autoimmune diabetes.
32	15833265	Most NKT cells express both an invariant T cell antigen receptor and the NK cell receptor NK1.1, and are referred to as invariant NKT cells.
33	15833265	This invariant T cell receptor is restricted to interactions with glycolipids presented by the non-classical MHC, CD1d.
34	15833265	These NKT cells rapidly produce high levels of interleukin (IL)-2, IFN-gamma, TNF-alpha, and IL-4 upon stimulation through their TCR.
35	15888910	Restoring the numerical and/or functional deficiency of iNKT cells in NOD mice by either treatment with alpha-galactosylceramide, transgenic induction of Valpha14-Jalpha18 expression, or transgenic expression of CD1d in NOD islets under the control of the human insulin promoter confers protection from T1D in these mice.
36	15944310	Lack of chemokine receptor CCR5 promotes murine fulminant liver failure by preventing the apoptosis of activated CD1d-restricted NKT cells.
37	15944310	In this study, we demonstrate that CCR5 deficiency promotes the development of acute FLF in mice following Con A administration by preventing activated hepatic CD1d-restricted NKT cells (but not conventional T cells) from dying from activation-induced apoptosis.
38	15944310	The resistance of CCR5-deficient NKT cells from activation-induced apoptosis following Con A administration is not due to a defective Fas-driven death pathway.
39	15944310	Moreover, FLF in CCR5-deficient mice also correlated with hepatic CCR5-deficient NKT cells, producing more IL-4, but not IFN-gamma, relative to wild-type NKT cells.
40	15944310	Lack of chemokine receptor CCR5 promotes murine fulminant liver failure by preventing the apoptosis of activated CD1d-restricted NKT cells.
41	15944310	In this study, we demonstrate that CCR5 deficiency promotes the development of acute FLF in mice following Con A administration by preventing activated hepatic CD1d-restricted NKT cells (but not conventional T cells) from dying from activation-induced apoptosis.
42	15944310	The resistance of CCR5-deficient NKT cells from activation-induced apoptosis following Con A administration is not due to a defective Fas-driven death pathway.
43	15944310	Moreover, FLF in CCR5-deficient mice also correlated with hepatic CCR5-deficient NKT cells, producing more IL-4, but not IFN-gamma, relative to wild-type NKT cells.
44	16177088	From 451 T cell clones from control and diabetic PLN, we derived 55 iNKT cells by two methods and analyzed function by cytokine secretion. iNKT cell clones isolated from control PLN secreted IL-4 and IFN-gamma upon TCR stimulation.
45	16177088	For type 1a diabetic subjects, PLN iNKT cell clones from three samples secreted IFN-gamma and no IL-4.
46	16177088	From normal and diabetic PLN, one-third of CD1d tetramer+-sorted T cell clones were reactive with CD1d transfectants or proliferated/secreted cytokine in response to alpha-galactosylceramide-pulsed PBMCs; tetramer-staining T cell clones from diabetic PLN did not secrete IL-4.
47	16178791	Unlike conventional T cells that recognize peptides in association with major histocompatibility complex (MHC), NKT cells recognize glycolipid antigens presented by the non-polymorphic MHC class I-like protein, CD1d.
48	16178791	Recently, we and other groups have demonstrated that administration of glycolipid ligands such as alpha-galactosylceramide (alpha-GC ) or its sphingosine truncated derivative, OCH suppressed autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE), diabetes in NOD mice and collagen-induced arthritis (CIA) by inducing T helper (Th) 2 bias of autoimmune T cells.
49	16178791	OCH is a unique ligand to stimulate NKT cells to selectively produce Th2 cytokines whereas alpha-GC induces both interleukin (IL)-4 and interferon (IFN)-gamma, and is more beneficial for treatment of a wide variety of Th1-mediated autoimmune diseases.
50	16412042	The non-classical antigen presenting molecule CD1d presents lipids and glycolipids to this highly specialized subset of T lymphocytes found in both humans and mice.
51	16505600	iNKT cells are a unique subset of CD1-restricted T lymphocytes that express T cell receptor (TCR) and some NK receptors. iNKT cells express an invariant TCRalpha chain composed of Valpha14-Jalpha18 segments in mice and Valpha24-Jalpha18 segments in humans associated with TCRbeta chains using a restricted set of Vbeta. iNKT cells recognize glycolipid antigens such as alpha-galactosylceramide (alpha-GC) presented by CD1d, non-pormorphic MHC class I-like molecule, and rapidly secrete large amounts of cytokines including IL-4 and IFN-gamma upon activation.
52	16809320	Interaction of antigen-presenting cell CD1d with distinct natural killer T-cell ("NKT") populations can induce rapid gamma interferon (IFN-gamma) production and NK-cell activation.
53	16809320	However, this was not reflected in the relative levels of NK-cell activation but rather by the responses of both CD4(+) and CD8(+) T-cell populations.
54	16809320	Repeated EMCV infection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenocytes than with the wild type.
55	16809320	Interaction of antigen-presenting cell CD1d with distinct natural killer T-cell ("NKT") populations can induce rapid gamma interferon (IFN-gamma) production and NK-cell activation.
56	16809320	However, this was not reflected in the relative levels of NK-cell activation but rather by the responses of both CD4(+) and CD8(+) T-cell populations.
57	16809320	Repeated EMCV infection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenocytes than with the wild type.
58	17100636	NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (Valpha14-Jalpha28).
59	17100636	Activation of NKT lymphocytes leads to rapid amplification of either IFNgamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses.
60	17100636	Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice.
61	17100636	NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes.
62	17100636	On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation.
63	17100636	NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (Valpha14-Jalpha28).
64	17100636	Activation of NKT lymphocytes leads to rapid amplification of either IFNgamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses.
65	17100636	Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice.
66	17100636	NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes.
67	17100636	On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation.
68	17100636	NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (Valpha14-Jalpha28).
69	17100636	Activation of NKT lymphocytes leads to rapid amplification of either IFNgamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses.
70	17100636	Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice.
71	17100636	NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes.
72	17100636	On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation.
73	17600041	Natural killer T (NKT) cells are a subset of regulatory T lymphocytes that recognize glycolipid antigens presented by the major histocompatibility complex class I-related glycoprotein CD1d.
74	18295332	Here we show that antibodies to CD1d, when given during early thymic development, induce specific increases in surface TCR of developing NOD and C57BL/6 CD4(+)CD8(+) (DP) invariant NKT (iNKT) cells.
75	18465023	Cooperation of invariant NKT cells and CD4+CD25+ T regulatory cells in prevention of autoimmune diabetes in non-obese diabetic mice treated with alpha-galactosylceramide.
76	18465023	CD1d-restricted natural killer T (NKT) cells and CD4+CD25+ regulatory T (Treg) cells are two thymus-derived subsets of regulatory T cells that play an important role in the maintenance of self-tolerance.
77	18465023	Yet the functional changes of the two subsets of regulatory T cells in the development of diabetes in non-obese diabetic (NOD) mice remain unclear, and how NKT cells and CD4+CD25+ Treg cells cooperate functionally in the regulation of autoimmune diabetes is also uncertain.
78	18465023	We provide evidence that in NOD mice, an animal model of human type 1 diabetes, the functions of both NKT cells and CD4+CD25+ Treg cells decrease in an age-dependent manner.
79	18465023	We show that treatment with alpha-galactosylceramide increases the size of the CD4+CD25+ Treg cell compartment in NOD mice, and augments the expression of forkhead/winged helix transcription factor and the potency of CD4+CD25+ Treg cells to inhibit proliferation of CD4+CD25- T cells.
80	18465023	Our data indicate that NKT cells and CD4+CD25+ Treg cells might cooperate in the prevention of autoimmune diabetes in NOD mice treated with alpha-galactosylceramide.
81	18465023	Induced cooperation of NKT cells and CD4+CD25+ Treg cells could serve as a strategy to treat human autoimmune disease, such as type 1 diabetes.
82	21078913	The different iNKT cell effects are mediated through distinct mechanisms and activation of different molecular pathways within the DC: CD1d signaling and activation of the ERK1/2 pathway for the tolerogenic action, and CD40-CD40L interaction and NF-κB activation for the adjuvant effect.
83	23527709	Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1.
84	23527709	Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits.
85	23527709	In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged.
86	23527709	These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice.
87	23527709	Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes.
88	23527709	Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1.
89	23527709	Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits.
90	23527709	In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged.
91	23527709	These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice.
92	23527709	Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes.
93	23527709	Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1.
94	23527709	Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits.
95	23527709	In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged.
96	23527709	These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice.
97	23527709	Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes.
98	23527709	Splenocytes from adult db/db and CD1d-knockout mice of both genders and their wild-type, C57BL/6 and Balb/C counterparts were examined for tumor necrosis factor (TNF)-alpha and TNF-alpha receptor type 1.
99	23527709	Despite the absence of inflammatory infiltrates, the hearts of db/db mice showed alterations in TNF-alpha receptor-1 and NFkB activity, including increased expression of both the NFkB p52 and p65 subunits.
100	23527709	In the hearts of CD1d-knockout mice, p52 expression was reduced, while p65 expression remained largely unchanged.
101	23527709	These results provide evidence for CD1d-mediated NFkB activation and diastolic dysfunction in the hearts of db/db mice.
102	23527709	Therefore, CD1d-associated abnormalities of innate immune responses and TNF-alpha production in splenic tissue may contribute to NFkB activation and cardiac dysfunction in type 2 diabetes.