ROLE OF TH17 CELLS IN LUNG INFLAMMATION: MODULATION BY OZONE AND ENVIRONMENTAL T

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 呼吸道上皮持续暴露于各种空气传播的抗原中，因此必须做好准备以防止病原体对呼吸道上皮细胞的定植。粘膜表面由分泌性IgA(SIgA)介导的一线防御保护，SIgA位于呼吸道粘膜纤毛层内，在那里SIgA发挥其抗原中和的保护功能。上皮细胞在维持气道中的IgA水平方面起着关键作用，因为它们在基底部表达聚合免疫球蛋白受体(PIgR)，该受体有助于二聚体IgA和IgM向心尖表面的跨细胞转运。虽然已经发表了大量关于肠道上皮和衍生细胞系诱导pIgR的药物的信息，但对于调节其在小鼠呼吸道中表达的因素知之甚少。新的证据表明，产生IL-17的Th17细胞在黏膜宿主防御各种微生物方面发挥关键作用。IL-17与中性粒细胞的募集和随后的细胞外微生物的根除有关。此外，最近有报道称，IL-17与IL-22协同作用，增强与宿主防御相关的抗菌肽的表达，如防御素2。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The epithelium of the respiratory tract is persistently exposed to a myriad of airborne antigens and must therefore be poised to prevent epithelial colonization by pathogenic agents. Mucosal surfaces are protected by a first-line defense mediated by secretory IgA (SIgA) that is contained within the muco-ciliary layer lining the airway, where SIgA exerts its protective function of antigen neutralization. Epithelial cells play a critical role in maintaining IgA levels in the airway since they express the polymeric immunoglobulin receptor (pIgR) basolaterally that serves to facilitate the transcytosis of dimeric IgA and IgM to the apical surface. Although a wealth of information has been published regarding the range of agents that serve to induce pIgR by intestinal epithelium and derived cell lines, very little is known as to the factors that regulate its expression in the mouse airway. Emerging evidence suggests that IL-17-producing Th17 cells play key roles in mucosal host defense against diverse microbes. IL-17 has been implicated in the recruitment of neutrophils and subsequent eradication of extracellular microorganisms. Moreover, IL-17 has recently been reported to cooperate with IL-22 to enhance the expression of antimicrobial peptides that are associated with host defense, such as ¿-defensin 2.