Although the etiology of sarcoidosis is still unknown, characteristic morphologic aspects and immunohistological patterns of sarcoid granulomatous lesions suggest that they are the consequence of an exaggerated immunological response against an undefined antigen which persists at different sites of disease involvement. This article reviews the newly emerging hypothesis regarding the molecular bases which drive the development of sarcoid granulomas. The accumulation of Th1 cells represents the pivotal step along the series of events that lead to the formation of granuloma; furthermore, a set of biological mediators of the immune response define immune regulatory networks that may contribute to tissue damage. It is also thought that shifts of the Th1/Th2 networks and alterations in the complex networks between immunocompetent cells and mesenchymal cells may set the stage for the remodeling of tissues surrounding granulomatous lesions.