The pancreatic-duct system was observed during the initial stage of ty
pe 1 diabetes in C57BL/6J mice rendered diabetic with low doses of str
eptozocin. Light microscopy revealed that the ducts located in close p
roximity to islets (islet ducts) were involved in the infiltrating pro
cess: inflammatory cells extended from the islets to these ducts. Howe
ver, ducts that were located far from islets (non-islet ducts) were ge
nerally free from infiltration. Immunocytochemistry revealed that both
islet ducts and non-islet ducts express MHC class II and ICAM-1 molec
ules: this positivity seems to be mainly expressed by elements infiltr
ating the connective layer or by endothelia of vessels surrounding duc
ts. Strong ICAM-1 positivity demonstrates that adhesiveness is widely
represented in early diabetes in this animal model. At the ultrastruct
ural level only a few endocrine elements were observed scattered withi
n the epithelial layer and single infiltrating elements were rarely en
countered within the connective layer of ducts. The existence of other
sites of <<activation>> other than the islets of Langerhans, in this
as well as in other animal models of types 1 diabetes, is consistent w
ith the hypothesis of an initially more widespread and less specific p
rocess that later undergoes restriction.