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Apoptosis: One of the Mechanisms That Maintains Unresponsiveness of the Intestinal Mucosal Immune System¹

Ping Bu^2,*, Ali Keshavarzian^2,, David D. Stone^2,*, Jianzhong Liu^*, Phong T. Le, Susan Fisher and Liang Qiao^3,*

Departments of ^* Microbiology and Immunology, Medicine, and Cell Biology, Neurobiology and Anatomy, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153; and Division of Digestive Diseases, Rush University, Chicago, IL 60612

Intestinal mucosa is constantly exposed to environmental Ags. Activation of lamina propria (LP) T cells by luminal Ags may lead to the production of inflammatory cytokines and subsequent mucosal inflammation and tissue damage. However, in normal circumstances, LP T cells do not respond to antigenic stimulation. The mechanisms of this unresponsiveness in healthy subjects are not fully understood. In this study, we found by in vivo analysis that, except for T cells in lymph nodules of the mucosa, 15% of LP T cells underwent apoptosis in normal individuals. In contrast, there was a marked reduction in apoptosis of LP T cells in patients with inflammatory bowel disease (Crohn’s disease and ulcerative colitis) and those with specific colitis. Our findings suggest that apoptosis might be a mechanism that turns off mucosal T cell responses to environmental Ags in healthy subjects, and resistance to apoptosis could be an important cause of mucosal immune dysregulation and tissue inflammation in colitis.

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