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Chain–deficient Mice
Correspondence to: Hiroshi Kiyono, Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan. Tel:81-6-6879-8294 Fax:81-6-6878-6765 E-mail:kiyono{at}biken.osaka-u.ac.jp.
T cell receptor chain–deficient (TCR--/-) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ßß (CD4+ßß) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ßß T cells, we treated TCR--/- mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR--/- mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR--/- mice treated with either specific or mock Ab developed CD4+ßß T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon 
–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ßß T cells play a major immunopathological role in the induction of IBD in TCR--/- mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ßß T cells to shift to the Th1 type.
Key Words:
inflammatory bowel disease, T cell receptor chain–deficient mice, interleukin 4, mucosal immunity, pathogenic T cell, Th2-induced colitis
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