The evolution of Mycobacterium tuberculosis as an intracellular pathogen has led to a complex relationship between it and its host, the human mononuclear phagocyte. The products of M. tuberculosis-specific T lymphocytes are essential for macrophage activation for intracellular mycobacterial killing. However, some cytokines, including products of both lymphocytes and phagocytic cells, may contribute to enhanced mycobacterial survival and replication. In human immunodeficiency virus-associated tuberculosis, cytokine products may mediate enhanced susceptibility to tuberculosis as well as accelerated progression to AIDS. Better understanding of these interactions will allow the development of increasingly specific immune-based interventions for prevention and treatment of tuberculosis.
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