Abstract
Background: Sarcoidosis is thought to arise from an exaggerated Th1/Th17-response upon exposure to unidentified antigens in susceptible individuals. Failure of the immunosuppressive function of regulatory T cells (Tregs) has been reported to contribute to an ongoing and uncontrolled response in sarcoidosis, leading to the characteristic granuloma formation and T cell alveolitis. Importantly, it remains unknown what underlying mechanisms cause functional deficits of the Tregs in sarcoidosis. Therefore, the primary objective of this study is to identify defects in Tregs of pulmonary sarcoidosis patients.
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