T-helper-17 (TH17) cells play a critical role in mucosal defense and autoimmune disease pathogenesis. They are most abundant in the small intestine lamina propria, where their presence requires colonization of mice with microbiota. Segmented filamentous bacteria (SFB) are sufficient to induce TH17 cells and to promote TH17-dependent autoimmune disease in animal models.

These TCR transgenic mice (derived from clone 1A2) were created to investigate the mechanisms by which distinct bacteria induce the specificity of TH17 cells and foster tissue-specific inflammation. Animals express V&alpha;15 /V&beta;14 CDR3 sequences which recognize SFB epitope QFSGAVPNK under the control of the natural TCR&alpha; and -&beta; promoter/enhancer elements. SFB-specific T cells become TH17 cells in SFB-colonized mice. Over 90% CD4+ T cells from the peripheral blood are TCRV&beta;14+ by FACS analysis (as compared to a typical less than 10% for control mice).

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T cells from these TCR transgenic mice recognize intestinal segmented filamentous bacteria (SFB) and predominantly become TH17 cells in SFB-colonized mice. These mice, derived from clone 1A2, are useful in studies of the relationship between commensal microbiota and organ-specific autoimmunity.

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C57BL/6J-Tg(Tcra Tcrb)3Litt/J Frozen Embryo