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Protection of the intestinal mucosa by intraepithelial γδ T cells

机译:上皮内γδT细胞对肠粘膜的保护

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摘要

γδ intraepithelial T lymphocytes (IEL) represent a major T cell population within the intestine of unclear functional relevance. The role of intestinal γδ IEL was evaluated in the dextran sodium sulfate (DSS) induced mouse colitis model system. Large numbers of γδ T cells, but not αβ T cells, were localized at sites of DSS-induced epithelial cell damage. γδ IEL in DSS treated mice expressed keratinocyte growth factor (KGF), a potent intestinal epithelial cell mitogen. γδ cell-deficient mice (TCRδ~(-/-)) and KGF-deficient mice (KGF~(-/-)), but not αβ cell-deficient mice (TCRα~(-/-)), 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 TCRδ~(-/-) mice or KGF~(-/-) mice. These results suggest that γδ IEL help preserve the integrity of damaged epithelial surfaces by providing the localized delivery of an epithelial cell growth factor.
机译:γδ上皮内T淋巴细胞(IEL)代表功能相关性不清楚的肠内主要T细胞群体。在葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎模型系统中评估了肠道γδIEL的作用。大量的γδT细胞而不是αβT细胞位于DSS诱导的上皮细胞损伤的部位。 DSS处理的小鼠中的γδIEL表达了角质形成细胞生长因子(KGF),这是一种有效的肠上皮细胞有丝分裂原。 γδ细胞缺陷小鼠(TCRδ〜(-/-))和KGF缺陷小鼠(KGF〜(-/-))而非αβ细胞缺陷小鼠(TCRα〜(-/-))比野生型小鼠遭受DSS诱导的粘膜损伤,并在终止DSS治疗后表现出延迟的组织修复。 DSS治疗的终止导致野生型小鼠中剧烈的上皮细胞增殖,而在TCRδ-(-/-)小鼠或KGF-(-/-)小鼠中没有。这些结果表明,γδIEL通过提供上皮细胞生长因子的局部递送来帮助保留受损上皮表面的完整性。

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