Although the etiology of sarcoidosis is still unknown, characteristic
morphologic aspects and immunohistological patterns of sarcoid granulo
matous 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 newl
y emerging hypothesis regarding the molecular bases which drive the de
velopment of sarcoid granulomas. The accumulation of Th1 cells represe
nts the pivotal step along the series of events that lead to the forma
tion of granuloma; furthermore, a set of biological mediators of the i
mmune response define immune regulatory networks that may contribute t
o tissue damage. It is also thought that shifts of the Th1/Th2 network
s and alterations in the complex networks between immunocompetent cell
s and mesenchymal cells may set the stage for the remodeling of tissue
s surrounding granulomatous lesions.