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T cell-associated CD18 but not CD62L, ICAM-1, or PSGL-1 is required for the induction of chronic colitis

Departments of ¹Molecular and Cellular Physiology and ²Pathology, Louisiana State University Health Sciences Center, Shreveport, Louisiana

Submitted 14 December 2006 ; accepted in final form 27 February 2007

The induction and perpetuation of chronic colitis are thought to involve a complex set of adhesive interactions between T cells and endothelial cells located on the vasculature within secondary lymphoid tissue and the intestine. The objective of this study was to assess the roles of T cell-associated CD18, CD62L (L-selectin), ICAM-1, and P-selectin glycoprotein ligand-1 (PSGL-1) in the induction of chronic colitis in mice. CD4⁺CD25^– T cells derived from either wild-type (WT), CD18-deficient [CD18 knockout (KO)], CD62L KO, ICAM-1 KO, or PSGL-1 KO mice were adoptively transferred into recombinase activating gene-1 (RAG-1)-deficient mice (RAG KO mice) to assess the potential of these T cells to induce chronic colitis. At 8–10 wk following T cell transfer, we observed moderate to severe colitis as assessed by increases in colon weight-to-length ratios and by blinded histopathological analysis. In contrast, we found that transfer of CD18 KO T cells into RAG KO recipients resulted in the significant attenuation of colonic inflammation in these mice. Furthermore, we observed fewer infiltrating CD4⁺ T cells in the colonic lamina propria in the CD18 KORAG KO group compared with the WTRAG KO group. Finally, message levels of colonic TNF-, IL-1, and IFN- were significantly reduced in CD18 KORAG KO mice compared with colitic control animals. We conclude that T cell-associated CD18, but not CD62L, ICAM-1, or PSGL-1, is required for the development of chronic colitis.

T cell trafficking; inflammation; inflammatory bowel disease; cytokines; intracellular adhesion molecule-1; P-selectin glycoprotein ligand-1

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