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Interferon-Gamma, the Activated Macrophage, and Host Defense Against Microbial Challenge

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Grant support: US Public Health Service (NIH) grants AI 21510 and AI 16963.

▸Requests for reprints should be addressed to Henry W. Murray, M.D.; Room A-423, Cornell University Medical College, 1300 York Avenue; New York, New York 10021.

New York, New York

© 1988 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1988;108(4):595-608. doi:10.7326/0003-4819-108-4-595
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Recent research on human macrophage activation has reemphasized the critical role of the lymphokine-secreting T cell in converting quiescent macrophages to efficient microbicidal phagocytes. Interferon-gamma, a key lymphokine secreted by antigen-triggered T4+ helper cells, is capable of inducing the macrophage to act against a diverse group of microbial targets, in particular, intracellular pathogens. In animal models, treatment with recombinant interferon-gamma is beneficial in systemic intracellular infections, and inhibition of endogenous interferon-gamma activity impairs host resistance. Trials in patients with cancer, leprosy, and the acquired immunodeficiency syndrome (AIDS) have shown that interferon-gamma can activate the mononuclear phagocyte in humans. This research and the identification of patients whose T cells fail to produce interferon-gamma properly has set the stage for evaluating the role of macrophage-activating immunotherapy using interferongamma in various human infectious diseases.





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