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，提示IEL可能具有一种新的屏障功能，并在IEL和EC之间进行通讯。艾美耳球虫是导致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。探讨IEL在艾美耳球虫(Eimeria spp.)上皮屏障调节中的作用。为了对抗艾美耳球虫(E.vermiformis，E.vermiformis)的感染，我们展示了IEL的两个不同的作用：产生细胞因子以诱导保护性免疫，以及表达连接分子以保护上皮屏障。当卵囊W产量达到峰值时，IEL的数量明显增加。在感染过程中，IEL可增加干扰素-γ和肿瘤坏死因子-α的产生，降低转化生长因子-β的表达。制作。加入干扰素-γ和肿瘤坏死因子-α或从蠕形埃希氏菌感染小鼠的IEL获得的培养上清液可降低小鼠肠源性上皮细胞系CMT93细胞单层的跨上皮电阻(TER)，但抗这些细胞因子的抗体可抑制TER的下降。此外，转化生长因子-β可减轻干扰素-γ和肿瘤坏死因子-α引起的上皮单层损伤和TER的变化。在蠕形虫感染的小鼠中，当IEL产生高水平的干扰素-γ和肿瘤坏死因子-α，以及低水平的转化生长因子-β时，EC表达的连接分子减少。有趣的是，IEL持续表达连接分子，EC与IEL的共培养增加。这些结果表明，IEL不仅通过细胞因子的产生保护上皮细胞免受蠕形埃希菌诱导的改变，而且当EC内连接下调时，IEL还直接与上皮屏障相互作用。

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.