The pancreatic-duct system was observed during the initial stage of type 1 diabetes in C57BLI6J mice rendered diabetic with low doses of streptozocin. Light microscopy revealed that the ducts located in close proximity to islets (islet ducts) were involved in the infiltrating process: inflammatory cells extended from the islets to these ducts. However, ducts that were located far from islets (non-islet ducts) were generally free from infiltration. Immunocytochemistry revealed that both islet ducts and non-islet ducts express MHC class I1 and ICAM-l molecules: this positivity seems to be mainly expressed by elements infiltrating the connective layer or by endothelia of vessels surrounding ducts. Strong ICAM-l positivity demonstrates that adhesiveness is widely represented in early diabetes in this animal model. At the ultrastructural level only a few endocrine elements were observed scattered within the epithelia1 layer and single infiltrating elements were rarely encountered within the connective layer of ducts. The existence of other sites of ccactivation>>o ther than the islets of Langerhans, in this as well as in other animal models of types 1 diabetes, is consistent with the hypothesis of an initially more widespread and less specific process that later undergoes restriction.
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