The pathology of the endocrine pancreas in type 1 (insulin-dependent) diabetes mellitus
Abstract
Type 1 diabetes is an organ-specific autoimmune disease in which the insulin-secreting B cell is destroyed. Both genetic factors (linked to class II MHC genes) and environmental agents (viruses, diet) appear to be involved in the aetiology. Study of autopsy pancreases of children who die at presentation of their disease has proved elucidating. In such pancreases islets before, during and after B cell destruction, are all visible. The earliest defined immunological event in the disease process appears to be expression of interferon-alpha by insulin-containing B cells. Secretion of this cytokine is associated with hyperexpression of class I MHC by all the endocrine cells within insulin-containing islets. Another immunological phenomenon which is unique to type I diabetes is the presence of aberrant class II MHC molecule expression by B cells. This may induce autoimmunity by allowing antigen presentation of B cell specific antigens. If the onset of the disease process is marked by interferon-alpha expression by B cells then a search for the presence of a continuing viral infection in these cells may prove profitable, although no viruses have been found in them to date.
References
HLA-DQ beta gene contributes to susceptibility and resistance to insulin-dependent diabetes mellitus
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