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Alteration of V Usage and Cytokine Production of CD4⁺ TCR Homodimer T Cells by Elimination of Bacteroides vulgatus Prevents Colitis in TCR -Chain-Deficient Mice¹

Daisuke Kishi^*,, Ichiro Takahashi^*, Yasuyuki Kai^*,, Hiroshi Tamagawa^*,, Hideki Iijima^*, Suguru Obunai^*,, Riichiro Nezu, Toshinori Ito, Hikaru Matsuda and Hiroshi Kiyono^2,*

^* Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; and Division of General and Gastroenterological Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

A major pathogenic factor for the development of inflammatory bowel disease (IBD) is the breakdown of the intestinal homeostasis between the host immune system and the luminal microenvironment. To assess the potential influence of luminal Ags on the development of IBD, we fed TCR ^-/- mice an elemental diet (ED). ED-fed TCR ^-/- mice showed no pathologic features of IBD, and their aberrant mucosal B cell responses were suppressed. Similar numbers of CD4⁺, TCR homodimer T cells ( T cells) were developed in the colonic mucosa of ED-fed mice; however, Th2-type cytokine productions were lower than those seen in diseased regular diet (RD)-fed mice. The higher cytokine production in diseased RD-fed mice could be attributed to the high incidence of Bacteroides vulgatus (recovered in 80% of these mice), which can induce Th2-type responses of colonic CD4⁺, T cells. In contrast, ED-fed TCR ^-/- mice exhibited a diversification of V usage of T cell populations from the dominant V8 one associated with B. vulgatus in cecal flora to V6, V11, and V14. Rectal administration of disease-free ED-fed mice with B. vulgatus resulted in the development of Th2-type CD4⁺, T cell-induced colitis. These findings suggest that the ED-induced alteration of intestinal microenvironments such as the enteric flora prevented the development of IBD in TCR ^-/- mice via the immunologic quiescence of CD4⁺, T cells.

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