Characterization of pancreatic islet cell infiltrates in NOD mice: effect of cell transfer and transgene expression

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Abstract
Insulin‐dependent diabetes mellitus can be transferred into young irradiated non‐obese diabetic (NOD) mice by spleen cells from a diabetic NOD donor. T cells (both L3T4+ and Ly‐2+) enter the pancreas 2 weeks following transfer. They are present initially at peri‐islet locations but progressively infiltrate the islet with accompanying β cell destruction. The infiltrate is heterogeneous with respect to Vβ usage. Inflammatory macrophages (Mac‐1+, F4/80+) can be detected at peri‐islet locations at 1 week after transfer and continue to be recruited during the disease process. Their presence at the initiation of disease suggests that their primary function may be autoantigen presentation. Increased expression of major histocompatibility complex (MHC) class I molecules is observed on both endocrine and exocrine tissue in areas of infra‐islet infiltration. MHC class II and ICAM‐1 expression was restricted to the cells constituting the inflammatory infiltrate. Expression of these molecules was not observed on β cells implying that presentation of autoantigen by the β cell itself does not play a role in the β cell destruction in NOD mice.