Abstract
Sarcoidosis is a disease of immune cell dysfunction. This review serves to amalgamate the information available into a coherent hypothesis. Recent research has shown that sarcoidosis should not be considered an antigenic induced granulomatous disease alone. The contribution of activation of auto immunity also has to be recognised. The triggering antigens have been narrowed mostly to be derived from Mycobacterial tubercular proteins and Propionobacter acnes. It is possible that they may share a common particle that creates a conformational change in the receptors of Th-1 cells that drives the disease until there is switch to autoimmunity and subsequent development of fibrosis. The role of genetic and environmental factors is also reviewed in this context.