THE HARDERIAN-GLAND IN AUTOIMMUNE DIABETES OF THE NONOBESE DIABETIC MOUSE

Infiltration of the nonobese diabetic (NOD) mouse's Harderian gland (H G) was studied in 1-30-week-old animals. A mononuclear cell invasion o f this gland is first seen in 8-week-old female mice (i.e., at a sligh tly later age than that for the onset of infiltration of pancreatic is lets). Infiltrating elements are mainly located at the hilus of the gl and or at one or two foci (periacinar infiltration) within the parench yma. In the latter case, a few elements infiltrate the fibrous connect ive tissue surrounding the acini (one or more) without damaging them. The most severe histopathological lesion was observed in 16-week-old a nimals; 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 p arenchyma is substituted with infiltrating elements, fibroblasts, and connective tissue. HG infiltration is comparable to the pancreatic inf lammatory infiltration; the two processes are very similar, though ins ulitis starts slightly earlier than HG infiltration. Furthermore, as f or insulitis and diabetes incidence, HG infiltration affects NOD males less than females. Moreover, immunocytochemistry has shown that T lym phocytes are the prevalent infiltrating element both in pancreatic isl ets and HGs. Further studies are required to understand the reasons fo r autoimmune destruction of this gland. (C) 1996 Wiley-Liss, Inc.