The function of intestinal intraepithelial T lymphocytes for repair of epithelial barrier during challenge with the coccidial pathogen Eimeria spp.

位于上皮细胞（EC）基底外侧部位的IEL。我们发现，IEL表达连接分子，occludin和E-cadherin EC，这表明IEL的一个新的屏障功能和IEL和EC之间的通信的可能性。艾美耳球虫属是引起球虫病的细胞内原生动物寄生虫。IEL对艾美耳球虫具有免疫调节和免疫保护作用。感染目的探讨IEL在艾美耳球虫感染过程中对上皮屏障的调节作用。感染，我们证明了两个不同的作用IEL对感染蠕虫型艾美耳球虫（E。蠕虫状），一种鼠病原体;产生细胞因子以诱导保护性免疫和表达连接分子以保护上皮屏障。当卵囊W产量达到高峰时，IEL的数量显著增加。在感染过程中，IEL增加IFN-γ和TNF-α的产生，降低TGF-β的产生。生产加入IFN-γ和TNF-α或从E.蠕虫感染的小鼠降低了融合的CMT 93细胞单层（一种鼠膀胱衍生的上皮细胞系）的跨上皮电阻（TER），但针对这些细胞因子的抗体抑制了TER的下降。TGF-β还能减轻IFN-γ和TNF-α引起的上皮细胞单层损伤和TER的变化。当IEL产生高水平的IFN-γ和TNF-α，低水平的TGF-β时，EC连接分子的表达减少。蠕虫感染的小鼠。有趣的是，IEL不断表达连接分子，EC与IEL共培养增加TER。这些结果表明，IEL发挥重要的多功能的作用，不仅在保护上皮细胞对E蠕虫引起的细胞因子的产生的变化，但也直接与上皮屏障的相互作用时，EC内连接下调。

IEL that reside at the basolateral site of epithelial cells (EC). We found that IEL express junctional molecules, occludin and E-cadherin EC, suggesting possibility of a novel barrier function of IEL and communication between IEL and EC. Eimeria spp.' are intracellular protozoan parasite that cause coccidiosis. IEL have been suggested to have immunoregulatory and immunoprotective roles against Eimeria spp. infection. To investigate how IEL are involved in the regulation of epithelial barrier during Eimeria spp. infection, we demonstrated two distinct roles of IEL against infection with Eimeria vermiformis (E. vermiformis), a murine pathogen; production of cytokines to induce protective immunity and expression of junctional molecules to preserve epithelial barrier. The number of IEL markedly increased when oocyst W production reached a peak. During infection, IEL increased production of IFN-γ and TNF-α and decreased TGF-β. production. Addition of IFN-γ and TNF-α or supematants obtained from cultured IEL from E. vermiformis-infected mice reduced transepithelial electrical resistance (TER) in confluent CMT93 cell monolayer, a murine intestinal-derived epithelial line, but antibodies against these cytokines suppressed the decline of TER. Moreover, TGF-β attenuates the damage of epithelial monolayer and changes in TER caused by IFN-γ and TNF-α. The expression of junctional molecules by EC was decreased when IEL produced a high level of IFN-γ and TNF-α, and a low level of TGF-β in E. vermiformis-infected mice. Interestingly, IEL constantly expressed junctional molecules and a co-culture of EC with IEL increased TER. These results suggest that IEL play important multi-functional roles not only in protection of the epithelium against E vermiformis-induced change by cytokine production but also direct interaction with the epithelial barrier when intra-EC junctions are down-regulated.