Sarcoidosis continues to be a disease of research interest because of its complicated immune mechanisms and elusive etiology. So far, it has been established that granulomatous inflammation in sarcoidosis is predominantly a T-helper 1 immune response mediated by a complex network of lymphocytes, macrophages, and cytokines. The cause of progression to a chronic and potentially fibrotic form is unclear but may involve loss of apoptotic mechanisms, loss of regulatory response, or a persistent antigen that cannot be cleared. Recent genomic and proteomic technology has emphasized the importance of host susceptibility and gene-environment interaction in the expression of the disease.