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.
Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice.
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S Trembleau, G Penna, E Bosi, A Mortara, M K Gately, L Adorini; Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes in NOD mice.. J Exp Med 1 February 1995; 181 (2): 817–821. doi: https://doi.org/10.1084/jem.181.2.817
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