Although there have been numerous reports on the isolation of bacteria, fungus, and aetiological agents of chemical substances from specimens of patients with sarcoidosis, none of them have been substantiated. In any event, an understanding of the pathogenesis of pulmonary sarcoid is intimately linked to that of the processes involved in the accumulation of T-cells in the lower respiratory tract of individuals with sarcoidosis. Propionibacterium acnes was isolated at high rates and in high concetrations from lymph nodes in patients with sarcoidosis. However, the precise mechanism of granuloma formation and immunomodulation by P. acnes has not been elucidated yet. In patients with sarcoidosis, it was found that the high levels of interleukin-2 (IL-2) released from alveolar lymphocytes as well as interleukin-1, tumor necrosis factor (TNF) and interleukin-6 (IL-6) released from alveolar macrophages were stimulated by P. acnes. These cytokines (mainly IL-2), released by P. acnes in large quantities, play a major role in the compartmentalization of the T-cell population in the lung and lead to the formation of an alveolitis and granuloma in the lung parenchyma of patients with sarcoidosis. This paper focuses primarily on the role of the cytokine network in the pulmonary mononuclear cells in the lung of patients with sarcoidosis.