Abstract
There is ample evidence for the involvement of IFN-γ in the formation of epithelioid cell granulomas, which are characteristic to sarcoid lesions. However, sarcoidosis does not belong to a typical Th1-type immune pathophysiology, in which only IFN-γ is working. It has a complex aspect in that IL-4 and other cytokines are involved depending on the stages and lesions of the disease. Upstream pathways have recently been elucidated which lead to the induction of IFN-γ. IL-12 and IL-18 are, among other things, play principal roles. Roles of IL-12 in sarcoidosis have already been documented, however, those of IL-18 have remained to be elucidated. Gene polymorphisms of IFN-γ, related cytokines, and signal transducing proteins may affect the occurrence and clinical course of sarcoidosis by modulating the production of IFN-γ.
