Ignet

Gene Information

Gene symbol: ART2P

Gene name: ADP-ribosyltransferase 2 (RT6 antigen homolog, rat) pseudogene

HGNC ID: 724

Related Genes

#	Gene Symbol	Number of hits
1	AGRP	1 hits
2	ART1	1 hits
3	ART3	1 hits
4	CD200	1 hits
5	CD4	1 hits
6	CD5	1 hits
7	CD8A	1 hits
8	FGF4	1 hits
9	GPI	1 hits
10	HBB	1 hits
11	HSD11B1	1 hits
12	IDDM2	1 hits
13	IFNG	1 hits
14	IL1B	1 hits
15	IL2	1 hits
16	IL4	1 hits
17	INS	1 hits
18	KLRB1	1 hits
19	LCK	1 hits
20	OMP	1 hits
21	PLCB1	1 hits
22	PLCG1	1 hits
23	SH2D1A	1 hits
24	THY1	1 hits
25	TNF	1 hits
26	TRA	1 hits
27	TYR	1 hits

Related Sentences

#	PMID	Sentence
1	1446803	In this generation of animals, 24% were lymphopenic with decreased numbers of PBL expressing CD5, TCR alpha, and RT6.
2	1446803	Moreover, IEL of the lymphopenic animals exhibited a pattern of staining (increased numbers of TCR alpha beta+CD4+CD8+ and decreased numbers of TCR alpha beta+CD4-CD8+) similar to that of BB DP animals.
3	1707018	Diabetes-prone (DP) BB rats develop spontaneous autoimmune insulin-dependent diabetes mellitus (IDDM).
4	1707018	Diabetes-resistant (DR) BB rats that are depleted of RT6+ T lymphocytes also become diabetic and provide an additional model of IDDM.
5	1707018	We report that diabetes in DR rats depleted of RT6+ T lymphocytes is prevented by the concomitant depletion of either the CD5+ or the CD8+ population.
6	1707018	Diabetes-prone (DP) BB rats develop spontaneous autoimmune insulin-dependent diabetes mellitus (IDDM).
7	1707018	Diabetes-resistant (DR) BB rats that are depleted of RT6+ T lymphocytes also become diabetic and provide an additional model of IDDM.
8	1707018	We report that diabetes in DR rats depleted of RT6+ T lymphocytes is prevented by the concomitant depletion of either the CD5+ or the CD8+ population.
9	1716208	Treatment with a phosphatidylinositol (PI)-specific phospholipase C markedly reduced the RT6 density showing that PI-mediated anchoring of RT6 in the cell membrane also applies to IEL of DP BB rats.
10	1864483	Insulin treatment prevents diabetes mellitus but not thyroiditis in RT6-depleted diabetes resistant BB/Wor rats.
11	1864483	This study investigated the effect of insulin treatment on the development of overt diabetes, clinically inapparent anti-islet autoreactivity, and thyroiditis in RT6-depleted diabetes resistant BB rats.
12	1864483	We conclude that insulin treatment prevents clinical diabetes in the RT6-depleted diabetes resistant BB rat, but this treatment does not prevent the development of autoreactive cell populations that cause thyroiditis and adoptively transfer diabetes.
13	1864483	Insulin treatment prevents diabetes mellitus but not thyroiditis in RT6-depleted diabetes resistant BB/Wor rats.
14	1864483	This study investigated the effect of insulin treatment on the development of overt diabetes, clinically inapparent anti-islet autoreactivity, and thyroiditis in RT6-depleted diabetes resistant BB rats.
15	1864483	We conclude that insulin treatment prevents clinical diabetes in the RT6-depleted diabetes resistant BB rat, but this treatment does not prevent the development of autoreactive cell populations that cause thyroiditis and adoptively transfer diabetes.
16	1864483	Insulin treatment prevents diabetes mellitus but not thyroiditis in RT6-depleted diabetes resistant BB/Wor rats.
17	1864483	This study investigated the effect of insulin treatment on the development of overt diabetes, clinically inapparent anti-islet autoreactivity, and thyroiditis in RT6-depleted diabetes resistant BB rats.
18	1864483	We conclude that insulin treatment prevents clinical diabetes in the RT6-depleted diabetes resistant BB rat, but this treatment does not prevent the development of autoreactive cell populations that cause thyroiditis and adoptively transfer diabetes.
19	2018977	Of particular interest was the RT6+ T cell subset, that appears to have important immunoregulatory properties in a rat model of autoimmune insulin-dependent diabetes mellitus.
20	2018977	Analysis of other lymphocyte subpopulations demonstrated a decrease of CD4+ and CD5+ cells, whereas B cells as well as CD8+, IL-2 receptor+, and MHC class II+ subsets showed no consistent correlation with the onset or resolution of the autoimmune process.
21	2210079	In these studies, PI-phospholipase C (PLC) treatment of lymphocytes from BB and normal rats followed by immunoabsorption and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of released proteins with anti-RT6 allotype-specific monoclonal antibodies was performed.
22	2210079	In contrast, no evidence of either RT6 species was found after PLC or detergent treatment of comparable numbers of T lymphocytes from DP-BB rats.
23	2533758	In addition, a number of other immune abnormalities have been observed, like severe T lymphopenia, lack of CD8+ T cells, and lack of RT6+ T cells.
24	2533758	Since both RT6 and MRC OX-32 antigens are only expressed by mature peripheral T cells, it is tempting to speculate that the peripheral T cell pool of DP BB rats consists only of immature peripheral T cells, i.e. recent thymic emigrants.
25	2533758	In addition, a number of other immune abnormalities have been observed, like severe T lymphopenia, lack of CD8+ T cells, and lack of RT6+ T cells.
26	2533758	Since both RT6 and MRC OX-32 antigens are only expressed by mature peripheral T cells, it is tempting to speculate that the peripheral T cell pool of DP BB rats consists only of immature peripheral T cells, i.e. recent thymic emigrants.
27	2567683	Nonlymphopenic parental, F1, and F2 rats revealed normal lymphocyte subsets, including CD8+ and RT6+ T-lymphocytes.
28	2567683	Lymphopenic parental and F2 rats revealed the absence of CD8+ and RT6+ cells, indicating that these T-lymphocyte abnormalities of lymphopenic DP rats segregate with the lymphopenia gene.
29	2567683	Nonlymphopenic parental, F1, and F2 rats revealed normal lymphocyte subsets, including CD8+ and RT6+ T-lymphocytes.
30	2567683	Lymphopenic parental and F2 rats revealed the absence of CD8+ and RT6+ cells, indicating that these T-lymphocyte abnormalities of lymphopenic DP rats segregate with the lymphopenia gene.
31	3058800	Lymphocyte transfusion experiments and in vivo depletion studies have demonstrated that RT6+ T cells have an important regulatory role in the pathogenesis of insulin-dependent diabetes mellitus in BB/Wor rats.
32	3058800	Inasmuch as DP bone marrow can transfer the susceptibility for diabetes to irradiated recipients, our present results suggest that an important predisposing factor for insulin-dependent diabetes mellitus in DP rats is the inability of DP prothymocytes to generate RT6+ T cells.
33	3058800	Lymphocyte transfusion experiments and in vivo depletion studies have demonstrated that RT6+ T cells have an important regulatory role in the pathogenesis of insulin-dependent diabetes mellitus in BB/Wor rats.
34	3058800	Inasmuch as DP bone marrow can transfer the susceptibility for diabetes to irradiated recipients, our present results suggest that an important predisposing factor for insulin-dependent diabetes mellitus in DP rats is the inability of DP prothymocytes to generate RT6+ T cells.
35	7888038	Adoptive transfer of autoimmune diabetes mellitus to athymic rats: synergy of CD4+ and CD8+ T cells and prevention by RT6+ T cells.
36	7888038	We describe the induction and prevention of autoimmune insulin dependent diabetes mellitus (IDDM), and its pathological substrate, insulitis, in congenitally athymic nude rats following injections of major histocompatibility complex (MHC) compatible lymph node T cells.
37	7888038	It was also observed that both CD4+ and CD8+ T cells are required for efficient transfer of autoimmunity.
38	7888038	The data indicate that, as in the NOD mouse, a synergistic interaction between CD4+ and CD8+ T cells is important for beta cell destruction.
39	7930594	Flow cytometric analysis showed that BNY-2 cells were positive for CD4 and CD5 and were negative for CD8 and RT6, indicating that these cells were phenotypically Th cells rather than cytotoxic T cells. mAbs against rat MHC class II Ags (anti-RT1.D) blocked the proliferation response of BNY-2 cells, suggesting that these cells recognize the MHC class II Du molecule.
40	8094734	Diabetes in these lymphopoenic rats was associated with extensive insulitis involving CD4+ and CD8+ T cells and macrophages.
41	8094734	The autoimmune diabetes and insulitis were completely prevented by the injection of a particular CD4+ T cell subset, isolated from healthy syngeneic donors, of the phenotype CD45RClow T cell receptor alpha/beta+ RT6+ Thy-1- OX-40-.
42	8094734	Cells of this protective phenotype, which make up about 5% of thoracic duct lymphocytes, were found to provide help for secondary antibody responses and produce interleukin 2 (IL-2) and IL-4, but no interferon gamma, on in vitro activation.
43	8254201	DP rats are severely deficient in certain T cell subsets including CD8+ cytotoxic T cells (Tc) and RT6+ T cells.
44	8288246	Using PCR screening of human/rodent somatic cell hybrids and fluorescence in situ hybridization, we have determined that the gene for the human RT6 homologue is located at 11q13, centromeric to the gene for tyrosinase (TYR, albino locus) and telomeric to that for fibroblast growth factor 4 (FGF4).
45	8288246	The data suggest that the human RT6 gene constitutes a new linkage group with TYR and the gene for olfactory marker protein (OMP) on 11q, which has a counterpart in mouse chromosome 7.
46	8288246	Thus, in the human, the RT6 locus is dissociated from the hemoglobin beta chain locus (HBB) and its neighboring conserved linkage group at 11p15, in contrast to the mouse, in which RT6 shows a tighter linkage to Hbb than to Tyr.
47	8288246	Using PCR screening of human/rodent somatic cell hybrids and fluorescence in situ hybridization, we have determined that the gene for the human RT6 homologue is located at 11q13, centromeric to the gene for tyrosinase (TYR, albino locus) and telomeric to that for fibroblast growth factor 4 (FGF4).
48	8288246	The data suggest that the human RT6 gene constitutes a new linkage group with TYR and the gene for olfactory marker protein (OMP) on 11q, which has a counterpart in mouse chromosome 7.
49	8288246	Thus, in the human, the RT6 locus is dissociated from the hemoglobin beta chain locus (HBB) and its neighboring conserved linkage group at 11p15, in contrast to the mouse, in which RT6 shows a tighter linkage to Hbb than to Tyr.
50	8288246	Using PCR screening of human/rodent somatic cell hybrids and fluorescence in situ hybridization, we have determined that the gene for the human RT6 homologue is located at 11q13, centromeric to the gene for tyrosinase (TYR, albino locus) and telomeric to that for fibroblast growth factor 4 (FGF4).
51	8288246	The data suggest that the human RT6 gene constitutes a new linkage group with TYR and the gene for olfactory marker protein (OMP) on 11q, which has a counterpart in mouse chromosome 7.
52	8288246	Thus, in the human, the RT6 locus is dissociated from the hemoglobin beta chain locus (HBB) and its neighboring conserved linkage group at 11p15, in contrast to the mouse, in which RT6 shows a tighter linkage to Hbb than to Tyr.
53	8423330	One such process is insulitis, the pancreatic islet inflammation that leads to autoimmune insulin-dependent diabetes mellitus (IDDM).
54	8423330	It was acquired before the onset of insulitis but subsided after the onset of diabetes. 3) In contrast, neither unsorted total T cells nor in vitro-purified RT6- T cells activated EC. 4) Older DR rats depleted of RT6+ T cells did not become diabetic and their RT6- T cells did not activate EC. 5) T cell IFN-gamma production correlated with the intensity of EC activation. 6) direct T cell-EC contact was required for maximal IFN-gamma production and EC activation.
55	8558012	IFN-gamma and IL-12p40 mRNA increase with age in both diabetic and insulin-treated nondiabetic BB rats.
56	8558012	In both DP and RT6-depleted DR rats, IFN-gamma mRNA was present in islets before and during disease onset.
57	8558012	IL-2 and IL-4 mRNAs were minimal or undetectable in infiltrated islets but present in activated peripheral T cells.
58	8558012	Similar cytokine mRNA profiles were observed in the thyroids of RT6-depleted DR rats and in the islets of DP rats treated with prophylactic parenteral insulin to prevent diabetes.
59	8558012	We conclude that IFN-gamma and IL-12 may play a major role in the expression of insulitis and thyroiditis in the BB rat, that Th1 lymphocytes may predominate over Th2 lymphocytes in these inflammatory lesions, and that prevention of diabetes by insulin is not associated with an alteration in the cytokine gene profile of islet infiltrating cells.
60	8558012	IFN-gamma and IL-12p40 mRNA increase with age in both diabetic and insulin-treated nondiabetic BB rats.
61	8558012	In both DP and RT6-depleted DR rats, IFN-gamma mRNA was present in islets before and during disease onset.
62	8558012	IL-2 and IL-4 mRNAs were minimal or undetectable in infiltrated islets but present in activated peripheral T cells.
63	8558012	Similar cytokine mRNA profiles were observed in the thyroids of RT6-depleted DR rats and in the islets of DP rats treated with prophylactic parenteral insulin to prevent diabetes.
64	8558012	We conclude that IFN-gamma and IL-12 may play a major role in the expression of insulitis and thyroiditis in the BB rat, that Th1 lymphocytes may predominate over Th2 lymphocytes in these inflammatory lesions, and that prevention of diabetes by insulin is not associated with an alteration in the cytokine gene profile of islet infiltrating cells.
65	8669109	Diabetes-prone (DP) BB rats (RT1(u), RT6.1) spontaneously develop insulin-dependent diabetes mellitus (IDDM) and the disease manifestation resembles that in human IDDM.
66	8669109	To prevent the recurrence of IDDM in the grafts, monoclonal antibodies to intercellular adhesion molecule-1 and leukocyte function-associated antigen-1 were administered.
67	8669109	These findings demonstrated that stable macrochimerism of donor-derived RT6+ T cells could restore the immune responses and prevent the recurrence of IDDM in the DP recipients.
68	8669488	Diabetes-prone BB rats are deficient in peripheral RT6+ T cells and develop spontaneous autoimmune insulin-dependent diabetes mellitus.
69	8669488	Diabetes-resistant BB rats have normal numbers of RT6+ T cells, and insulin-dependent diabetes mellitus can be induced in these animals by in vivo depletion of peripheral RT6+ cells.
70	8669488	Diabetes-prone BB rats are deficient in peripheral RT6+ T cells and develop spontaneous autoimmune insulin-dependent diabetes mellitus.
71	8669488	Diabetes-resistant BB rats have normal numbers of RT6+ T cells, and insulin-dependent diabetes mellitus can be induced in these animals by in vivo depletion of peripheral RT6+ cells.
72	8757323	Recently, the T cell differentiation marker RT6 has been shown to possess mono-ADP-ribosyltransferase activity.
73	8757323	Defects in RT6 expression coincide with increased susceptibility in animal models for insulin-dependent diabetes mellitus and other autoimmune diseases.
74	8757323	Recently, the T cell differentiation marker RT6 has been shown to possess mono-ADP-ribosyltransferase activity.
75	8757323	Defects in RT6 expression coincide with increased susceptibility in animal models for insulin-dependent diabetes mellitus and other autoimmune diseases.
76	8816966	Th1 cytokines are thought to play a key role in islet inflammation and destruction in insulin-dependent diabetes mellitus (IDDM).
77	8816966	In contrast, expression of message for IL-2 and IL-4 is minimal to undetectable in DP-BB and RT6-depleted DR-BB animals at any age.
78	8816966	Incubation of 10 wk old DP islets for 48 h in the presence of anti-CD3 antibody, followed by an incubation with rIL-2 for an additional 5-7 days, results in an expansion of T lymphocytes, and these cells express high levels of IFN-gamma and IL-10 mRNA.
79	8816966	Our results suggest that autoimmunity in DP-BB and DR-BB rats is mediated by Th1 lymphocytes and that IFN-gamma and IL-12 are likely to play a key role in islet and thyroid inflammation and destruction in IDDM.
80	8826980	Antibody cross-linking of RT6 enhanced expression of the alpha subunit of the interleukin-2 (IL-2) receptor and potentiated the proliferation of rat T-cells cultured in the presence of phorbol ester plus recombinant IL-2 (rIL-2) and/or rIL-4.
81	8826980	RT6 was found to coimmunoprecipitate with five tyrosine phosphorylated proteins including p60fyn and p56lck, members of the src tyrosine kinase family.
82	8826980	Pretreatment of T-cells with phorbol ester increased the phosphorylation of proteins that coimmunoprecipitated with RT6, altered the electrophoretic mobility of several of these coimmunoprecipitated phosphoproteins, and increased the amount of p60fyn and p56lck coimmunoprecipitated with RT6.
83	8826980	Antibody cross-linking of RT6 enhanced expression of the alpha subunit of the interleukin-2 (IL-2) receptor and potentiated the proliferation of rat T-cells cultured in the presence of phorbol ester plus recombinant IL-2 (rIL-2) and/or rIL-4.
84	8826980	RT6 was found to coimmunoprecipitate with five tyrosine phosphorylated proteins including p60fyn and p56lck, members of the src tyrosine kinase family.
85	8826980	Pretreatment of T-cells with phorbol ester increased the phosphorylation of proteins that coimmunoprecipitated with RT6, altered the electrophoretic mobility of several of these coimmunoprecipitated phosphoproteins, and increased the amount of p60fyn and p56lck coimmunoprecipitated with RT6.
86	8826980	Antibody cross-linking of RT6 enhanced expression of the alpha subunit of the interleukin-2 (IL-2) receptor and potentiated the proliferation of rat T-cells cultured in the presence of phorbol ester plus recombinant IL-2 (rIL-2) and/or rIL-4.
87	8826980	RT6 was found to coimmunoprecipitate with five tyrosine phosphorylated proteins including p60fyn and p56lck, members of the src tyrosine kinase family.
88	8826980	Pretreatment of T-cells with phorbol ester increased the phosphorylation of proteins that coimmunoprecipitated with RT6, altered the electrophoretic mobility of several of these coimmunoprecipitated phosphoproteins, and increased the amount of p60fyn and p56lck coimmunoprecipitated with RT6.
89	8937686	Abnormalities in postthymic T cell development in the BB/W rat model of autoimmune insulin-dependent diabetes mellitus (IDDM) result in part from a lymphopenia (lyp) gene defect.
90	8937686	These results suggested that, at a minimum, an arrest in maturation of the Thy1+ precursors of RT6+ T cells occurs postthymically in DP rats.
91	8937686	The results showed that in DP, as compared with DR, rats: 1) 5-fold fewer RTE's are exported from the thymus per 24 hr; 2) more than 80% of the RTE's are CD4+; 3) most of the immediate descendants of RTE's disappear from the peripheral lymphoid tissues within one week after export from the thymus; and 4) few of the descendants of the RTE's that do survive differentiate into RT6+ T cells.
92	8937686	Abnormalities in postthymic T cell development in the BB/W rat model of autoimmune insulin-dependent diabetes mellitus (IDDM) result in part from a lymphopenia (lyp) gene defect.
93	8937686	These results suggested that, at a minimum, an arrest in maturation of the Thy1+ precursors of RT6+ T cells occurs postthymically in DP rats.
94	8937686	The results showed that in DP, as compared with DR, rats: 1) 5-fold fewer RTE's are exported from the thymus per 24 hr; 2) more than 80% of the RTE's are CD4+; 3) most of the immediate descendants of RTE's disappear from the peripheral lymphoid tissues within one week after export from the thymus; and 4) few of the descendants of the RTE's that do survive differentiate into RT6+ T cells.
95	8976193	Previous studies have shown that the disease is prevented by the intravenous injection of 5 x 10(6) CD4+ CD45RC-TCR alpha beta+ RT6+ peripheral T cells from normal syngeneic donors.
96	8976193	However, we now report that the CD4+ CD8- population of mature thymocytes is a very potent source of cells, with the capacity to prevent diabetes in our lymphopenic animals.
97	9193658	The percentage of RT6 positive cells was increased by in vitro stimulation of isolated NK cells with high concentrations of recombinant rat IL-2 indicating that RT6 expression may be associated with an activated state in NK cells.
98	9200647	Coisogenic diabetes-resistant (DR) BB/Wor rats do not develop diabetes spontaneously, but IDDM can readily be induced by treatment with polyinosinic:polycytidylic acid and depletion of RT6+ T-cells.
99	9243099	Lyp controls the number of peripheral lymphocytes by reducing T cells of the RT6+ phenotype by almost 90%.
100	9243099	The frequency of IFN gamma and interleukin (IL)-10 mRNA expressing cells in isolated thymocytes determined by quantitative image analysis, demonstrated an increased IFN gamma: IL-10 ratio in thymocytes from lyp/lyp homozygotes compared to lyp/+ and +/+ rats.
101	9243099	Recombinant human glutamic acid decarboxylase (GAD65) increased the number of IFN gamma and IL-10 mRNA expressing thymocytes after in vitro culture.
102	9300695	Rat T cells that express the ART designated RT6 are determinants of the expression of autoimmune diabetes.
103	9686581	Thy-1, another GPI-linked protein, and proteins that reacted with anti-GPI-oligosaccharide Abs also translocated from HDL to the nonlipoprotein fraction under similar conditions.
104	9686581	These data suggest that HDL is a carrier of plasma RT6 and other GPI-linked proteins, with equilibrium between the lipoprotein and nonlipoprotein fractions being salt dependent.
105	9686581	Since GPI-linked proteins in HDL can transfer to cells in a functionally active form, the presence of RT6 in HDL is consistent with it having a role in signaling in nonlymphoid cells.
106	9686581	Thy-1, another GPI-linked protein, and proteins that reacted with anti-GPI-oligosaccharide Abs also translocated from HDL to the nonlipoprotein fraction under similar conditions.
107	9686581	These data suggest that HDL is a carrier of plasma RT6 and other GPI-linked proteins, with equilibrium between the lipoprotein and nonlipoprotein fractions being salt dependent.
108	9686581	Since GPI-linked proteins in HDL can transfer to cells in a functionally active form, the presence of RT6 in HDL is consistent with it having a role in signaling in nonlymphoid cells.
109	9716913	It was found that strain-related susceptibility to diabetes induction correlated with a higher level of IL-2, IFN-gamma, and TNF-alpha production, whereas such differences were not observed when IL-1 and NO production by macrophages were analyzed; elimination of immunoregulatory RT6+T cells that increases IFN-gamma production, enhances susceptibility to MLD-STZ-induced diabetes; mercury-induced Th-2 cells down-regulated the disease; IFN-gamma-mediated macrophage activation to produce proinflammatory cytokines rather than NO is an important event in early diabetogenic effects of invading macrophages; inhibition of IL-1 activity downregulates diabetes induction; and generation of NO in beta cells appears to be important for diabetogenic effects.
110	9892610	Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes.
111	9892610	Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors.
112	9892610	RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells.
113	9892610	We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats.
114	9892610	The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4.
115	10201921	We report that cultured DR- and DP-BB rat thymi generate mature CD4 and CD8 single-positive cells with up-regulated TCRs.
116	10201921	In contrast, DP-BB rat cultures generate fewer CD4+, CD8+, and RT6+ T cells.
117	10331639	The RT6 (Art2) family of ADP-ribosyltransferases in rat and mouse.
118	10331639	Recent evidence suggests that a new member of the mono-ADP-ribosyltransferase/NAD glycohydrolase family, RT6, may be important in immune regulation.
119	10331639	RT6-expressing T cells in the rat may have a regulatory role, a conclusion based on their ability to prevent autoimmune diabetes in the BB rat model of insulin-dependent diabetes mellitus.
120	10331639	RT6, like many GPI-linked proteins, can mediate cell signal transduction events associated with T cell activation, and is also present in a soluble form in the circulation.
121	10331639	The RT6 (Art2) family of ADP-ribosyltransferases in rat and mouse.
122	10331639	Recent evidence suggests that a new member of the mono-ADP-ribosyltransferase/NAD glycohydrolase family, RT6, may be important in immune regulation.
123	10331639	RT6-expressing T cells in the rat may have a regulatory role, a conclusion based on their ability to prevent autoimmune diabetes in the BB rat model of insulin-dependent diabetes mellitus.
124	10331639	RT6, like many GPI-linked proteins, can mediate cell signal transduction events associated with T cell activation, and is also present in a soluble form in the circulation.
125	10331639	The RT6 (Art2) family of ADP-ribosyltransferases in rat and mouse.
126	10331639	Recent evidence suggests that a new member of the mono-ADP-ribosyltransferase/NAD glycohydrolase family, RT6, may be important in immune regulation.
127	10331639	RT6-expressing T cells in the rat may have a regulatory role, a conclusion based on their ability to prevent autoimmune diabetes in the BB rat model of insulin-dependent diabetes mellitus.
128	10331639	RT6, like many GPI-linked proteins, can mediate cell signal transduction events associated with T cell activation, and is also present in a soluble form in the circulation.
129	10331639	The RT6 (Art2) family of ADP-ribosyltransferases in rat and mouse.
130	10331639	Recent evidence suggests that a new member of the mono-ADP-ribosyltransferase/NAD glycohydrolase family, RT6, may be important in immune regulation.
131	10331639	RT6-expressing T cells in the rat may have a regulatory role, a conclusion based on their ability to prevent autoimmune diabetes in the BB rat model of insulin-dependent diabetes mellitus.
132	10331639	RT6, like many GPI-linked proteins, can mediate cell signal transduction events associated with T cell activation, and is also present in a soluble form in the circulation.
133	10593564	Both are used to model human insulin-dependent diabetes mellitus (IDDM).
134	10593564	We now report that the phenotype of NK T cells in the rat is alphabetaTcR+ CD8+ CD4-, comparable to the NK T cell phenotype reported for humans, which is alphabetaTcR+ CD4- Valpha24-JalphaQ, and either CD8- or CD8alphaalpha+.
135	10593564	Because RT6+ T cells are deficient in DP-BB rats, and because depletion of cells expressing RT6 induces IDDM in DR-BB rats, we studied NK T cells for expression of this antigen.
136	10919571	Importance of donor-derived lymphocytes in the protection of pancreaticoduodenal or islet grafts from recurrent autoimmunity: a role for RT6+NKR-P1+ T cells.
137	12794058	Given this hierarchical pattern in gene expression, the protein IGF-2 is more tolerated than INS.
138	12794058	This thymus-specific defect in Igf2 expression may explain both the absence of central tolerance to INS-secreting beta cells and the lymphopenia (including lack of regulatory RT6(+) T cells) in diabetes-prone BB rats.
139	12794058	INS B:9-23 and the homologous sequence of IGF-2 compete for binding to DQ8, an MHC class II allele conferring major susceptibility to T1DM.
140	12794058	In young DQ8(+) T1DM patients, INS B:9-23 presentation by DQ8 elicits a dominant IFN-gamma secretion by isolated PBMCs, whereas presentation of the IGF-2 self-antigen promotes a dominant regulatory interleukin-10 secretion.
141	12794058	These data demonstrate that opposite immune responses are driven by MHC presentation of a self-antigen (here, IGF-2) and an autoantigen (INS, as "altered" self).
142	14768945	BB rats showed a rapid preferential loss of CD8+ and CD45RC+ T cells, whereas the relative loss of RT6+ T cells was proportional to that of all T cells and not significantly different from that in PVG rats.