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The Journal of Immunology, 1999, 162: 1843-1850.
Copyright © 1999 by The American Association of Immunologists

Clonal Expansion of CD4+ TCRßß+ T Cells in TCR {alpha}-Chain- Deficient Mice by Gut-Derived Antigens1

Ichiro Takahashi2,*, Hideki Iijima*, Rumi Katashima{dagger}, Mitsuo Itakura{dagger} and Hiroshi Kiyono*

* Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; and {dagger} Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, University of Tokushima, Tokushima, Japan

A population of CD4+ {alpha}-ß+ T cells increases in the mucosal and peripheral lymphoid tissues of TCR{alpha}-chain-deficient mice with inflammatory bowel disease. The {alpha}-ß+ T cells, which produce predominantly IL-4, mediate the proliferation of colonic epithelial crypts and the infiltration of large numbers of IgA-producing plasma cells into the lamina propria of the colon. To examine whether enteric Ags were recognized by a population of monoclonal {alpha}-ß+ T cells leading to the intestinal inflammation, we examined the usage and clonotypes of TCR expressed by the {alpha}-ß+ T cells in TCR{alpha}-chain-deficient mice with inflammatory bowel disease. Analyses of immunoprecipitates by two dimensional electrophoresis and single-cell RT-PCR revealed that TCR of the {alpha}-ß+ T cells was a homodimer of ß-chains that was capable of recognizing luminal bacterial Ags. PCR single-strand conformation polymorphism analysis of TCR Vß transcripts revealed monoclonal accumulation of the {alpha}-ß+ T cells in the colonic lamina propria of the diseased mice. DNA sequencing revealed the accumulation of the {alpha}-ß+ T cells with the same CDR3 sequences in the colon. These findings suggest that the pathogenic CD4+ {alpha}-ß+ T cells expressing a homodimeric form of the TCRß-chains can be clonally expanded upon the stimulation with gut-derived Ags.




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