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Role of T Cells in the Inflammatory Response of Experimental Colitis Mice ¹

Takahiro Tsuchiya^2,*, Sumiaki Fukuda^*, Hiromasa Hamada^*,, Akihiro Nakamura^*, Yasuhiro Kohama^*, Hiromichi Ishikawa, Kazutake Tsujikawa^* and Hiroshi Yamamoto^3,*

^* Department of Immunology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan; and Department of Microbiology, Keio University School of Medicine, Tokyo, Japan

We examined the severity of experimental colitis induced by dextran sulfate sodium (DSS) using immunologically manipulated mice. C57BL/6 mice showed more severe colitis than BALB/c mice, but mice of both strains recovered fully from the disease after the removal of DSS from their drinking water. The infiltrated cells at the lesions were mainly granulocytes in normal littermates. However, C.B-17 scid, IL-7R deficient, and TCR-C double-deficient mice showed severe colitis and did not recover from the disease even after the removal of DSS. It was found that the infiltrated cells at the lesions in the lethal strains were monocytes. Although both TCR-C^-/- and TCR-C^-/- mice showed severe colitis phenotypes, infiltration in the former is monocyte-dominant while that in the latter is granulocyte-dominant. Thus the type of cells that infiltrate at the lesions of DSS-induced experimental colitis may be controlled by functional T cell subsets. Immunohistological and RT-PCR analyses of the inflamed colon revealed that the murine homologue of human GRO released by some cells under the control of T cells is a possible candidate determining the severity of DSS-induced experimental colitis.

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