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Publication : Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice.

First Author  Trembleau S Year  1995
Journal  J Exp Med Volume  181
Issue  2 Pages  817-21
PubMed ID  7836934 Mgi Jnum  J:22507
Mgi Id  MGI:70370 Doi  10.1084/jem.181.2.817
Citation  Trembleau S, et al. (1995) Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice. J Exp Med 181(2):817-21
abstractText  T cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. Administration of interleukin 12 (IL-12), a key cytokine which guides the development of T helper type 1 (Th1) CD4+ T cells, induces rapid onset of IDDM in NOD, but not in BALB/c mice. Histologically, IL-12 administration induces massive infiltration of lymphoid cells, mostly T cells, in the pancreatic islets of NOD mice. CD4+ pancreas-infiltrating T cells, after activation by insolubilized anti T cell receptor antibody, secrete high levels of interferon gamma and low levels of IL-4. Therefore, IL-12 administration accelerates IDDM development in genetically susceptible NOD mice, and this correlates with increased Th1 cytokine production by islet-infiltrating cells. These results hold implications for the pathogenesis, and possibly for the therapy of IDDM and of other Th1 cell-mediated autoimmune diseases.
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