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

TH17 细胞在肺部炎症中的作用：臭氧和环境 T 的调节

• 批准号: 7959567
• 负责人: ZEINA JAFFAR
• 金额: $ 1.18万
• 依托单位: UNIVERSITY OF MONTANA
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-06-01 至 2010-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7959567
• 关键词: Antigens; Apical; Cell Line; Cells; Computer Retrieval of Information on Scientific Projects Database; Defensins; Environmental Health; Epithelial; Epithelial Cells; Epithelium; Funding; Grant; Host Defense; Immunoglobulin A; Immunoglobulin M; Institution; Interleukin-17; Lung Inflammation; Mediating; Microbe; Mus; Neutrophil Infiltration; Ozone; Play; Polymeric Immunoglobulin Receptors; Publishing; Reporting; Research; Research Personnel; Resources; Respiratory System; Respiratory tract structure; Role; Secretory Immunoglobulin A; Source; Surface; United States National Institutes of Health; antimicrobial peptide; extracellular; interleukin-22; intestinal epithelium; microorganism; prevent; transcytosis

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 呼吸道的上皮持续暴露于无数的空气传播的抗原，因此必须准备好防止病原体的上皮定植。粘液表面受到由分泌型伊加（SIgA）介导的第一线防御的保护，所述分泌型IgA（SIgA）包含在衬于气道的粘膜纤毛层内，其中SIgA发挥其抗原中和的保护功能。上皮细胞在维持气道中的伊加水平中起关键作用，因为它们在基底外侧表达多聚免疫球蛋白受体（pIgR），所述多聚免疫球蛋白受体（pIgR）用于促进二聚伊加和IgM转胞吞至顶端表面。 尽管已经发表了大量关于通过肠上皮细胞和衍生细胞系诱导pIgR的试剂范围的信息，但是对于调节其在小鼠气道中表达的因子知之甚少。新出现的证据表明，IL-17产生的Th 17细胞在粘膜宿主防御不同微生物中发挥关键作用。IL-17与嗜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，IL-17最近被报道与IL-22合作以增强与宿主防御相关的抗微生物肽（例如防御素2）的表达。