| First Author | Tian J | Year | 1996 |
| Journal | Nat Med | Volume | 2 |
| Issue | 12 | Pages | 1348-53 |
| PubMed ID | 8946834 | Mgi Jnum | J:37023 |
| Mgi Id | MGI:84429 | Doi | 10.1038/nm1296-1348 |
| Citation | Tian J, et al. (1996) Modulating autoimmune responses to GAD inhibits disease progression and prolongs islet graft survival in diabetes-prone mice [see comments]. Nat Med 2(12):1348-53 |
| abstractText | In nonobese diabetic (NOD) mice, beta-cell reactive T-helper type 1 (Th1) responses develop spontaneously and gradually spread, creating a cascade of responses that ultimately destroys the beta-cells. The diversity of the autoreactive T-cell repertoire creates a major obstacle to the development of therapeutics. We show that even in the presence of established Th1 responses, it is possible to induce autoantigen-specific anti-inflammatory Th2 responses. Immune deviation of T-cell responses to the beta-cell autoantigen glutamate decarboxylase (GAD65), induced an active form of self-tolerance that was associated with an inhibition of disease progression in prediabetic mice and prolonged survival of syngeneic islet grafts in diabetic NOD mice. Thus, modulation of autoantigen-specific Th1/Th2 balances may provide a minimally invasive means of downregulating established pathogenic autoimmune responses. |
