Abstract

Sarcoidosis as a multisystemic inflammatory granulomatous disorder is characterized by local immune hyperactivation, inflammation, and granuloma formation. Many organs may be involved by sarcoidosis. The pathogenesis of sarcoidosis may be autoimmune response to an antigenic exposure. The lung is affected in the vast majority of patients, and common symptoms in lung sarcoidosis are nonproductive cough and dyspnea. The death cause is typically severe pulmonary complications, involvement of myocardia, and central nervous system. Sarcoid granuloma is comprised of epithelioid, mononuclear, and CD4+ T cells with a few CD8+ T cells. It was confirmed that there is association between HLA Class I and II genes as risk factors with sarcoidosis. Some alleles have protective effect against immunopathology of sarcoidosis, and some others are risk factor. The immune mechanisms of sarcoidosis are not completely understood. The inflammasome signal transductions pathway plays a critical role in sarcoidosis pathogenesis. Sarcoidosis treatment could potentially benefit from simultaneous modulation and fine-tuning of M2/Th2 and M1/Th1 pathways rather than targeting one pathway or the other. Future experimental investigations and clinical studies into sarcoidosis and all types of sarcoid reaction may increase our understanding.

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