期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2002
卷号：99
期号：22
页码：14338-14343
DOI：10.1073/pnas.212290499
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：{gamma}{delta} intraepithelial T lymphocytes (IEL) represent a major T cell population within the intestine of unclear functional relevance. The role of intestinal {gamma}{delta} IEL was evaluated in the dextran sodium sulfate (DSS) induced mouse colitis model system. Large numbers of {gamma}{delta} T cells, but not {beta} T cells, were localized at sites of DSS-induced epithelial cell damage. {gamma}{delta} IEL in DSS treated mice expressed keratinocyte growth factor (KGF), a potent intestinal epithelial cell mitogen. {gamma}{delta} cell-deficient mice (TCR{delta}-/-) and KGF-deficient mice (KGF-/-), but not {beta} cell-deficient mice (TCR-/-), were more prone than wild-type mice to DSS-induced mucosal injury and demonstrated delayed tissue repair after termination of DSS treatment. Termination of DSS treatment resulted in vigorous epithelial cell proliferation in wild-type mice but not in TCR{delta}-/- mice or KGF-/- mice. These results suggest that {gamma}{delta} IEL help preserve the integrity of damaged epithelial surfaces by providing the localized delivery of an epithelial cell growth factor.
