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The focus of my research is to study the role of the adaptive immune system in disease pathogenesis and to clearly define the mechanisms that regulate pathogenesis. By dissecting the host-cell interactions in granulomatous inflammation, I hope to identify host factors that may be exploited for novel therapies in chronic lung disease. Moreover, by investigating the role of individual cell subsets in granulomatous formation and maintenance, I hope to gain insight into how granulomatous inflammation is initiated and progresses to chronicity. Currently, I use sarcoidosis as a model system for granulomatous inflammation. Sarcoidosis is a unique disease which is at the crossroads of microbial infection and host immune response. Specifically, sarcoidosis is a multisystem granulomatous disease of unknown etiology, characterized by a T helper 1 (Th1) immunophenotype. Although sarcoidosis is a systemic disease, it most commonly affects the lungs. The immune response in sarcoidosis has been well characterized, however the lack of antigen has hindered in-depth analyses of the role of specific cells in sarcoidosis pathogenesis. Recent reports from independent laboratories have postulated mycobacteria as a candidate. The potential role of mycobacteria in sarcoidosis immunopathogenesis has been demonstrated by the detection of mycobacterial proteins and nucleic acids in sarcoidosis granulomas, as well as humoral and peripheral cellular immune responses to mycobacterial antigens in sarcoidosis subjects. In addition, our lab has made significant advances in studying the immune response to mycobacterial antigens at the site of active sarcoidosis involvement – the lungs. Our lab has demonstrated the presence of antigen-specific recognition of mycobacterial proteins in CD4+ and CD8+ T cells derived from sarcoidosis subjects at diagnostic bronchoscopy. The current focus is to delineate CD8+ molecular and biologic T cell function in sarcoidosis pathogenesis and how it influences sarcoidosis resolution or progression. In addition, we are interested in how HLA types correlate with disease outcome.

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    615-322-5266 (p)
    615-343-6160 (f)
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    Keywords

    granulomatous inflammation human immunology infectious disease sarcoidosis T lymphocytes