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Microsc Res Tech. 1996 Jun 1;34(2):156-65.

The harderian gland in autoimmune diabetes of the nonobese diabetic mouse.

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1
Institute of Anatomy, School of Medicine, Second University of Naples, Italy.

Abstract

Infiltration of the nonobese diabetic (NOD) mouse's Harderian gland (HG) was studied in 1-30-week-old animals. A mononuclear cell invasion of this gland is first seen in 8-week-old female mice (i.e., at a slightly later age than that for the onset of infiltration of pancreatic islets). Infiltrating elements are mainly located at the hilus of the gland or at one or two foci (periacinar infiltration) within the parenchyma. In the latter case, a few elements infiltrate the fibrous connective tissue surrounding the acini (one or more) without damaging them. The most severe histopathological lesion was observed in 16-week-old animals; at this time infiltration ranges from a still focal lesion to complete acinar destruction of the gland. Ultrastructural observations confirm that in several cases acinar cells are destroyed and the HG parenchyma is substituted with infiltrating elements, fibroblasts, and connective tissue. HG infiltration is comparable to the pancreatic inflammatory infiltration; the two processes are very similar, though insulitis starts slightly earlier than HG infiltration. Furthermore, as for insulitis and diabetes incidence, HG infiltration affects NOD males less than females. Moreover, immunocytochemistry has shown that T lymphocytes are the prevalent infiltrating element both in pancreatic islets and HGs. Further studies are required to understand the reasons for autoimmune destruction of this gland.

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