This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Chronic Rhinosinusitis (CRS) is a common disease affecting 15% of the general population and costing in excess of $6 billion annually. The pathogenesis of CRS is characterized by mucosal inflammation with activated epithelial cells and T cells. Nasal epithelial cells express B7 co-stimulatory molecules, specialized molecules that mediate T cell activation. These investigators hypothesize that inflammation associated with CRS alters the expression of B7 homologs and other specialized molecules that mediate the communication between epithelial cells and T cells. Furthermore, it is postulated that epithelial cell surface molecules can serve as markers of disease and that exacerbation of sinonasal disease will be associated with increased expression of epithelial co-stimulators. The overarching goal of this research is to understand the basic pathophysiology of CRS.
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