152 related articles for article (PubMed ID: 7948603)
1. GAD65 is recognized by T-cells, but not by antibodies from NOD-mice.
Bieg S; Seissler J; Herberg L; Northemann W; Scherbaum WA
Autoimmunity; 1994; 17(3):189-94. PubMed ID: 7948603
[TBL] [Abstract][Full Text] [Related]
2. Glutamic acid decarboxylase T lymphocyte responses associated with susceptibility or resistance to type I diabetes: analysis in disease discordant human twins, non-obese diabetic mice and HLA-DQ transgenic mice.
Boyton RJ; Lohmann T; Londei M; Kalbacher H; Halder T; Frater AJ; Douek DC; Leslie DG; Flavell RA; Altmann DM
Int Immunol; 1998 Dec; 10(12):1765-76. PubMed ID: 9885897
[TBL] [Abstract][Full Text] [Related]
3. Responses of NOD congenic mice to a glutamic acid decarboxylase-derived peptide.
Chen SL; Whiteley PJ; Freed DC; Rothbard JB; Peterson LB; Wicker LS
J Autoimmun; 1994 Oct; 7(5):635-41. PubMed ID: 7840855
[TBL] [Abstract][Full Text] [Related]
4. Major DQ8-restricted T-cell epitopes for human GAD65 mapped using human CD4, DQA1*0301, DQB1*0302 transgenic IA(null) NOD mice.
Liu J; Purdy LE; Rabinovitch S; Jevnikar AM; Elliott JF
Diabetes; 1999 Mar; 48(3):469-77. PubMed ID: 10078545
[TBL] [Abstract][Full Text] [Related]
5. Immunization with the larger isoform of mouse glutamic acid decarboxylase (GAD67) prevents autoimmune diabetes in NOD mice.
Elliott JF; Qin HY; Bhatti S; Smith DK; Singh RK; Dillon T; Lauzon J; Singh B
Diabetes; 1994 Dec; 43(12):1494-9. PubMed ID: 7525393
[TBL] [Abstract][Full Text] [Related]
6. Natural history of humoral immunity to glutamic acid decarboxylase in non-obese diabetic (NOD) mice.
De Aizpurua HJ; French MB; Chosich N; Harrison LC
J Autoimmun; 1994 Oct; 7(5):643-53. PubMed ID: 7840856
[TBL] [Abstract][Full Text] [Related]
7. Prevention of type I diabetes transfer by glutamic acid decarboxylase 65 peptide 206-220-specific T cells.
Kim SK; Tarbell KV; Sanna M; Vadeboncoeur M; Warganich T; Lee M; Davis M; McDevitt HO
Proc Natl Acad Sci U S A; 2004 Sep; 101(39):14204-9. PubMed ID: 15381770
[TBL] [Abstract][Full Text] [Related]
8. T cells with multiple fine specificities are used by non-obese diabetic (NOD) mice in the response to GAD(524-543).
Quinn A; Sercarz EE
J Autoimmun; 1996 Jun; 9(3):365-70. PubMed ID: 8816972
[TBL] [Abstract][Full Text] [Related]
9. Regulatory and effector CD4 T cells in nonobese diabetic mice recognize overlapping determinants on glutamic acid decarboxylase and use distinct V beta genes.
Quinn A; McInerney B; Reich EP; Kim O; Jensen KP; Sercarz EE
J Immunol; 2001 Mar; 166(5):2982-91. PubMed ID: 11207247
[TBL] [Abstract][Full Text] [Related]
10. Characterization of novel T-cell epitopes on 65 kDa and 67 kDa glutamic acid decarboxylase relevant in autoimmune responses in NOD mice.
Zechel MA; Elliott JF; Atkinson MA; Singh B
J Autoimmun; 1998 Feb; 11(1):83-95. PubMed ID: 9480726
[TBL] [Abstract][Full Text] [Related]
11. Widespread expression of an autoantigen-GAD65 transgene does not tolerize non-obese diabetic mice and can exacerbate disease.
Geng L; Solimena M; Flavell RA; Sherwin RS; Hayday AC
Proc Natl Acad Sci U S A; 1998 Aug; 95(17):10055-60. PubMed ID: 9707599
[TBL] [Abstract][Full Text] [Related]
12. Prevention of autoimmune diabetes by immunogene therapy using recombinant vaccinia virus expressing glutamic acid decarboxylase.
Jun HS; Chung YH; Han J; Kim A; Yoo SS; Sherwin RS; Yoon JW
Diabetologia; 2002 May; 45(5):668-76. PubMed ID: 12107747
[TBL] [Abstract][Full Text] [Related]
13. DNA vaccination with glutamic acid decarboxylase (GAD) generates a strong humoral immune response in BALB/c, C57BL/6, and in diabetes-prone NOD mice.
Wiest-Ladenburger U; Fortnagel A; Richter W; Reimann J; Boehm BO
Horm Metab Res; 1998 Oct; 30(10):605-9. PubMed ID: 9851666
[TBL] [Abstract][Full Text] [Related]
14. The clinical and immunological significance of GAD-specific autoantibody and T-cell responses in type 1 diabetes.
Boettler T; Pagni PP; Jaffe R; Cheng Y; Zerhouni P; von Herrath M
J Autoimmun; 2013 Aug; 44():40-8. PubMed ID: 23770292
[TBL] [Abstract][Full Text] [Related]
15. T cell proliferative responses to glutamic acid decarboxylase-65 in IDDM are negatively associated with HLA DR3/4.
Worsaae A; Hejnaes K; Moody A; Ludvigsson J; Pociot F; Lorenzen T; Dyrberg T
Autoimmunity; 1995; 22(3):183-9. PubMed ID: 8734572
[TBL] [Abstract][Full Text] [Related]
16. Identification of glutamic acid decarboxylase autoantibody heterogeneity and epitope regions in type I diabetes.
Ujihara N; Daw K; Gianani R; Boel E; Yu L; Powers AC
Diabetes; 1994 Aug; 43(8):968-75. PubMed ID: 8039604
[TBL] [Abstract][Full Text] [Related]
17. CD4(+) T cells from glutamic acid decarboxylase (GAD)65-specific T cell receptor transgenic mice are not diabetogenic and can delay diabetes transfer.
Tarbell KV; Lee M; Ranheim E; Chao CC; Sanna M; Kim SK; Dickie P; Teyton L; Davis M; McDevitt H
J Exp Med; 2002 Aug; 196(4):481-92. PubMed ID: 12186840
[TBL] [Abstract][Full Text] [Related]
18. Endogenous immune response to glutamic acid decarboxylase (GAD67) in NOD mice is modulated by adjuvant immunotherapy.
Qin HY; Elliott JF; Lakey JR; Rajotte RV; Singh B
J Autoimmun; 1998 Dec; 11(6):591-601. PubMed ID: 9878081
[TBL] [Abstract][Full Text] [Related]
19. Immunization of diabetes-prone or non-diabetes-prone mice with GAD65 does not induce diabetes or islet cell pathology.
Plesner A; Worsaae A; Dyrberg T; Gotfredsen C; Michelsen BK; Petersen JS
J Autoimmun; 1998 Aug; 11(4):335-41. PubMed ID: 9776711
[TBL] [Abstract][Full Text] [Related]
20. Transgenically induced GAD tolerance curtails the development of early beta-cell autoreactivities but causes the subsequent development of supernormal autoreactivities to other beta-cell antigens.
Tian J; Dang H; von Boehmer H; Jaeckel E; Kaufman DL
Diabetes; 2009 Dec; 58(12):2843-50. PubMed ID: 19741165
[TBL] [Abstract][Full Text] [Related]
[Next] [New Search]