Because of its association with cutaneous anergy, sarcoidosis was originally viewed as a defect of cellular immunity. Supporting that misperception were early studies of peripheral blood lymphocytes that found lymphopenia and impaired lymphocyte responses to mitogens and recall antigens. The clue to a vast underlying network of complex hyperactive cellular immune functions was discovered in the paradoxical finding of in vitro spontaneous lymphoblastic transformation and lymphokine production. Subsequently, investigative focus shifted to the activated, proliferating T-helper lymphocytes, the lymphokines of which were found to function in the recruitment and retention of monocytes for granuloma development. T-helper lymphocytes also contributed to the mechanism of hypergammaglobulinemia through their influence on B cells. The most intriguing question about sarcoid immunology is the initiating factor that triggers the T-lymphocyte activation and proliferation in the first place. There is much to suggest that antigen processing and presentation launches the process. Because lymphocyte activation and proliferation antedate granuloma formation at K-S skin test sites and in the lung, we combined the harvesting technique of BAL with the K-S bioassay to show that granulomagenic antigen is being processed by monocyte-macrophages. The finding of autologous monocyte-macrophage granulomagenicity raises the distinct possibility that sarcoidosis is a unique cell-mediated type of autoimmune process. The isolation and identification of the granulomagenic factor is the exciting research frontier ahead.