Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice.
作者： Sylvie Trembleau , Giuseppe Penna , Emanuele Bosi , Anna Mortara , Maurice K Gately
关键词: Endocrinology 、 Interleukin 21 、 Immunology 、 Interferon gamma 、 NOD mice 、 Biology 、 IL-2 receptor 、 Internal medicine 、 Interleukin 3 、 Interleukin 4 、 Interleukin 12 、 Nod
摘要: T cells play a major role in the development of insulin-dependent diabetes mellitus (IDDM) nonobese diabetic (NOD) mice. Administration interleukin 12 (IL-12), key cytokine which guides helper type 1 (Th1) CD4+ cells, induces rapid onset IDDM NOD, but not BALB/c Histologically, IL-12 administration massive infiltration lymphoid mostly pancreatic islets NOD pancreas-infiltrating after activation by insolubilized anti cell receptor antibody, secrete high levels interferon gamma and low IL-4. Therefore, accelerates genetically susceptible mice, this correlates with increased Th1 production islet-infiltrating cells. These results hold implications for pathogenesis, possibly therapy other cell-mediated autoimmune diseases.
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