Are T-cell responses to GAD65 influential in type 1 diabetes?

Diabetes

Volumn 58, Issue 12, 2009, Pages 2729-2730

  Quinn, Anthony ^a  

^a UNIVERSITY OF TOLEDO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELL ANTIGEN; GLUTAMATE DECARBOXYLASE 65;

ANTIGEN PRESENTING CELL; ANTIGEN SPECIFICITY; CELL SPECIFICITY; IMMUNE RESPONSE; INCIDENCE; INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; NOTE; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION; REGULATORY MECHANISM; T LYMPHOCYTE;

ANIMALS; DIABETES MELLITUS, TYPE 1; GLUTAMATE DECARBOXYLASE; INSULIN-SECRETING CELLS; MICE; MICE, INBRED NOD; T-LYMPHOCYTES;

EID: 73249123108     PISSN: 00121797     EISSN: 1939327X     Source Type: Journal    
DOI: 10.2337/db09-1445     Document Type: Note

References (19)

1. Delovitch TL, Singh B. The nonobese diabetic mouse as a model of autoimmune diabetes: immune dysregulation gets the NOD. Immunity 1997;7:727-738
2. Cahill GF Jr, McDevitt HO. Insulin-dependent diabetes mellitus: the initial lesion. N Engl J Med 1981;304:1454-1465
3. Cahill GF Jr. Diabetes mellitus: an overview. Curr Concepts Nutr 1981;10:145-151
4. Honeyman MC, Coulson BS, Stone NL, Gellert SA, Goldwater PN, Steele CE, Couper JJ, Tait BD, Colman PG, Harrison LC. Association between rotavirus infection and pancreatic islet autoimmunity in children at risk of developing type 1 diabetes. Diabetes 2000;49:1319-1324
5. Atkinson MA, Bowman MA, Campbell L, Darrow BL, Kaufman DL, Maclaren NK. Cellular immunity to a determinant common to glutamate decarboxylase and coxsackie virus in insulin-dependent diabetes. J Clin Invest 1994;94:2125-2129
6. Horwitz MS, Bradley LM, Harbertson J, Krahl T, Lee J, Sarvetnick N. Diabetes induced by Coxsackie virus: initiation by bystander damage and not molecular mimicry. Nat Med 1998;4:781-785
7. Turley S, Poirot L, Hattori M, Benoist C, Mathis D. Physiological beta cell death triggers priming of self-reactive T cells by dendritic cells in a type-1 diabetes model. J Exp Med 2003;198:1527-1537
8. Tisch R, Yang XD, Singer SM, Liblau RS, Fugger L, McDevitt HO. Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice. Nature 1993;366:72-75
9. Kaufman DL, Clare-Salzler M, Tian J, Forsthuber T, Ting GS, Robinson P, Atkinson MA, Sercarz EE, Tobin AJ, Lehmann PV. Spontaneous loss of T-cell tolerance to glutamic acid decarboxylase in murine insulin-dependent diabetes. Nature 1993;366:69-72
10. Nepom GT. Conversations with GAD. J Autoimmun 2003;20:195-198
11. Mallone R, Kochik SA, Laughlin EM, Gersuk VH, Reijonen H, Kwok WW, Nepom GT. Differential recognition and activation thresholds in human autoreactive GAD-specific T-cells. Diabetes 2004;53:971-977
12. Tian J, Clare-Salzler M, Herschenfeld A, Middleton B, Newman D, Mueller R, Arita S, Evans C, Atkinson MA, Mullen Y, Sarvetnick N, Tobin AJ, Lehmann PV, Kaufman DL. Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetesprone mice. Nat Med 1996;2:1348-1353
13. Jaeckel E, Klein L, Martin-Orozco N, von Boehmer H. Normal incidence of diabetes in NOD mice tolerant to glutamic acid decarboxylase. J Exp Med 2003;197:1635-1644
14. Tian J, Dang H, von Boehmer H, Jaeckel E, Kaufman DL. Transgenically induced GAD tolerance curtails the development of early β-cell autoreactivities but causes the subsequent development of supernormal autoreactivities to other β-cell antigens. Diabetes 2009;58:2843-2850
15. Yoon JW, Yoon CS, Lim HW, Huang QQ, Kang Y, Pyun KH, Hirasawa K, Sherwin RS, Jun HS. Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells. Science 1999;284:1183-1187
16. Geng L, Solimena M, Flavell RA, Sherwin RS, Hayday AC. Widespread expression of an autoantigen-GAD65 transgene does not tolerize nonobese diabetic mice and can exacerbate disease. Proc Natl Acad Sci U S A 1998;95:10055-10060
17. Kanazawa Y, Shimada A, Oikawa Y, Okubo Y, Tada A, Imai T, Miyazaki J, Itoh H. Induction of anti-whole GAD65 reactivity in vivo results in disease suppression in type 1 diabetes. J Autoimmun 2009;32:104-109
18. Christgau S, Schierbeck H, Aanstoot HJ, Aagaard L, Begley K, Kofod H, Hejnaes K, Baekkeskov S. Pancreatic beta cells express two autoantigenic forms of glutamic acid decarboxylase, a 65-kDa hydrophilic form and a 64-kDa amphiphilic form which can be both membrane-bound and soluble. J Biol Chem 1991;266:21257-21264
19. Kaufman DL, Houser CR, Tobin AJ. Two forms of the gamma-aminobutyric acid synthetic enzyme glutamate decarboxylase have distinct intraneuronal distributions and cofactor interactions. J Neurochem 1991;56:720-723