Free Content β7 Integrin expression is not required for the localization of T cells to the intestine and colitis pathogenesis

Authors: SYDORA, B. C.1; WAGNER, N.; LÖHLER, J.2; YAKOUB, G.1; KRONENBERG, M.3; MÜLLER, W.4; ARANDA, R.

Source: Clinical & Experimental Immunology, Volume 129, Number 1, July 2002 , pp. 35-42(8)

Publisher: Blackwell Publishing

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Abstract:

SUMMARY

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.

Keywords:  β7 integration colitis T cells trafficking

Document Type: Research article

DOI: 10.1046/j.1365-2249.2002.01892.x

Affiliations: 1: Division of Digestive Diseases, UCLA School of Medicine, USA, 2: Heinrich-Pette-Institute for Experimental Virology and Immunology, University of Hamburg, Germany, 3: La Jolla Institute of Allergy and Immunology, CA, USA, and 4: Institute for Genetics, University of Cologne, Germany,

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