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beta7 Integrin expression is not required for the localization of T cells to the intestine and colitis pathogenesis.

Abstract：

: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.

journal_name

Clin Exp Immunol

journal_title

Clinical and experimental immunology

authors

Sydora BC,Wagner N,Lohler J,Yakoub G,Kronenberg M,Muller W,Aranda R

doi

10.1046/j.1365-2249.2002.01892.x

subject

Has Abstract

pub_date

2002-07-01 00:00:00

pages

35-42

issue

1

eissn

0009-9104

issn

1365-2249

pii

1892

journal_volume

129

pub_type

杂志文章

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