β7 Integrin expression is not required for the localization of T cells to the intestine and colitis pathogenesis
β7 Integrins have been shown to have an important role in the localization of T cells to the intestine. Utilizing two different experimental mouse models of inflammatory bowel disease (IBD), this study was undertaken to determine if β7 integrin expression is critical for T cell localization to the intestine and colitis pathogenesis. Transfer of CD4+ CD45RBhigh cells into immunodeficient mice results in colitis. To examine the role of β7 integrins, donor cells were obtained from β7 integrin gene‐deficient animals and disease induction was examined following transfer into severe combined immunodeficiency (SCID) mice. Additionally, β7 integrin gene‐deficient animals were crossed to IL‐2‐deficient mice and the onset of spontaneous colitis that normally occurs in IL‐2‐deficient animals was examined. No differences in the onset or severity of spontaneous colitis was noted in animals that were deficient in both β7 integrin and IL‐2. In contrast, the onset of colitis in recipients of T cells from β7 integrin‐deficient donors was delayed significantly. In mice receiving β7 integrin negative cells, the initial lack of colitis appeared to correlate with fewer numbers of CD3+β7 integrin –/– donor lymphocytes present in the host colon. The eventual development of disease, however, was associated with increased numbers of donor β7 integrin –/– lymphocytes. These results show that β7 integrin expression is not absolutely required for T cell localization to the intestine and colitis pathogenesis.