Insulitis in human type 1 diabetes.
Pancreatic tissues were analyzed immunohistologically in patients with autoimmune and fulminant type 1 diabetes (T1D) and control subjects. Both beta and alpha cells were decreased in fulminant T1D, but only beta cells were significantly decreased in autoimmune T1D. Insulitis was seen in both subtypes of T1D, but it remained longer in autoimmune than in fulminant T1D. Lymphocytic infiltration to the exocrine pancreatic tissue was observed only in fulminant T1D, whereas immunologically abnormal findings, such as increased expression of MHC class I molecule and Fas antigen in islet cells and Fas-ligand expression in infiltrating lymphocytes, were detected only in autoimmune T1D. From these findings, together with clinical features, it could be concluded that in autoimmune T1D, beta cells are assumed to be destroyed through a long-standing autoimmune process, whereas in fulminant T1D, beta cells seem to be destroyed very rapidly, probably by a destructive process triggered by viral infection.
Hanafusa
Toshiaki
T
First Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan. hanafusa@poh.osaka-med.ac.jp
Imagawa
Akihisa
A
D001327:Autoimmune Diseases / Q000150:complications / Q000453:epidemiology / Q000276:immunology / Q000473:pathology; D001706:Biopsy; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000453:epidemiology* / Q000473:pathology; D016883:Diabetic Ketoacidosis / Q000276:immunology / Q000473:pathology; D006801:Humans; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D053583:Interleukin-1beta / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism; D008264:Macrophages / Q000473:pathology; D010195:Pancreatitis / Q000150:complications* / Q000453:epidemiology* / Q000276:immunology / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha