Abstract
The local inflammatory response in sarcoidosis appears to be a Th1-mediated process. Evidence exists that the systemic immune response, however, shows a Th2 predominance. Mycobacteria species, particularly cell wall-deficient forms, continue to be candidates for an infectious cause of the disease. Evidence for a possible role for human herpesvirus 8 has also been submitted. The relationship between sarcoidosis and infectious pathogens remains open to investigation. Both Sjögren's syndrome and common variable immunodeficiency display clinical and immunopathologic overlap with sarcoidosis. Blau's syndrome, a genetic disorder of autosomal dominant inheritance, may be confused with infantile sarcoidosis. Vasculitis in sarcoidosis may be underappreciated. Virtually any size vessel may be involved, thus adding to the multiplicity of clinical settings in which sarcoidosis can occur.
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