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

University Of Montana, Missoula MT

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Abstract

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 [unreadable]-defensin 2.