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(American Journal of Pathology. 2004;165:1849-1852.)
© 2004 American Society for Investigative Pathology

CD18 Deficiency Protects against Multiple Low-Dose Streptozotocin-Induced Diabetes

Shayne C. Barlow^*, Will Langston^*, Kametra M. Matthews, John H. Chidlow, Jr^* and Christopher G. Kevil^*

From the Departments of Molecular and Cellular Physiology^* and Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana

Leukocyte recruitment into pancreatic islets is believed to play an important pathophysiological role in autoimmune diabetes. Previous reports have suggested that several different adhesion molecules may be involved in leukocyte recruitment during autoimmune diabetes, including members of the leukocyte ß₂ integrins. Here we report that a gene-targeted deficiency of the ß₂ integrin, CD18, protects against multiple low-dose streptozotocin-induced autoimmune diabetes. CD18 null mice displayed lower blood glucose values throughout the study, with only 10% of these mice eventually developing diabetes compared to 95% in the control group. Importantly, the development of insulitis was markedly absent in the CD18 null mice, suggesting that members of this integrin subfamily predominately regulate leukocyte infiltration into pancreatic islets. This study demonstrates that the ß₂ integrins play a key pathophysiological role in the development of multiple low-dose streptozotocin-induced autoimmune diabetes.

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