Induction and perpetuation of chronic colitis is 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), intercellular adhesion molecule-1 (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 ko), CD62L ko, ICAM-1 ko or PSGL-1 ko mice were adoptively transferred into recombinase activating gene-1-deficient mice (RAG ko) to assess the potential of these T-cells to induce chronic colitis. At 8-10 weeks following T-cell transfer, we observed moderate to severe colitis in RAG ko mice reconstituted with WT, CD62L ko, ICAM-1 ko or PSGL-1 ko T-cells. 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 to the WTRAG ko. Finally, message levels of colonic TNF-, IL-1 and IFN- were reduced significantly in the CD18 koRAG ko mice when compared to the 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.