Pancreatic cellular infiltrates in autoimmune-prone New Zealand Black mice.

Healthy New Zealand Black (NZB) mice of both sexes (age 19-31 weeks) were studied to determine the magnitude of pancreatic beta cell injury related to mononuclear cell infiltration of islets. This investigation was undertaken following the description of spontaneous cellular immune reactions against islets in four strains of autoimmune-prone mice, including NZB mice [1]. Studies included complete autopsies with histological examination, determination of the pancreatic content of immunoreactive insulin, and the measurement of the plasma glucose concentration. Mononuclear cell infiltrates were identified in the lung, liver, kidney, salivary gland, mesentery, and pancreas. In the latter site, the infiltrates were situated in fibrous septae about ducts, ductules, and venules rather than islets. Only islets contiguous to infiltrates were involved, and then but focally. Insulitis, as manifest by the envelopment and permeation of islets by mononuclear cells, was not observed. In none was there a significant reduction of beta cells or pancreatic insulin content, neither was hyperglycaemia manifest. This study reveals that, although NZB mice are subject to autoimmune phenomena and widespread mononuclear cell infiltrates, beta cell injury and insulitis are not consistent features of this strain.