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Pulmonary tuberculosis is characterized by granulomatous inflammation with an extensive infiltration of mononuclear phagocytes, but the mechanisms of phagocyte recruitment to the pleural space is unknown. In this study, pleural fluid from patients with tuberculosis contained significantly (P < .001) more biologically active MIP-1α and MCP-1 (C-C cytokines) than did effusions from patients with congestive heart failure. Antigenic MIP-1α and MCP-1 was detected by immunocytochemistry in pleural biopsy sections of patients with tuberculous pleurisy. In vitro, pleural mesothelial cells stimulated with bacille Calmette-Guérin (BCG) or interferon (IFN)-γ produced MIP-1α and MCP-1. Reverse transcription-polymerase chain reaction studies confirmed that both BCG and IFN-γ induced MIP-1α and MCP-1 expression in mesothelial cells, demonstrating that mesothelial cell-derived C-C chemokines play a biologically important role in the recruitment of mononuclear cells to the pleural space.