| First Author | Sydora BC | Year | 2002 |
| Journal | Clin Exp Immunol | Volume | 129 |
| Issue | 1 | Pages | 35-42 |
| PubMed ID | 12100020 | Mgi Jnum | J:115570 |
| Mgi Id | MGI:3691938 | Doi | 10.1046/j.1365-2249.2002.01892.x |
| Citation | Sydora BC, et al. (2002) beta7 Integrin expression is not required for the localization of T cells to the intestine and colitis pathogenesis. Clin Exp Immunol 129(1):35-42 |
| abstractText | beta7 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 beta7 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 beta7 integrins, donor cells were obtained from beta7 integrin gene-deficient animals and disease induction was examined following transfer into severe combined immunodeficiency (SCID) mice. Additionally, beta7 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 beta7 integrin and IL-2. In contrast, the onset of colitis in recipients of T cells from beta7 integrin-deficient donors was delayed significantly. In mice receiving beta7 integrin negative cells, the initial lack of colitis appeared to correlate with fewer numbers of CD3+beta7 integrin -/- donor lymphocytes present in the host colon. The eventual development of disease, however, was associated with increased numbers of donor beta7 integrin -/- lymphocytes. These results show that beta7 integrin expression is not absolutely required for T cell localization to the intestine and colitis pathogenesis. |
