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Letters |15 June 1996

Interferon-γ and Management of Infectious Diseases

Steven M. Holland, MD; Joshua M. Farber, MD; John I. Gallin, MD

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  • National Institute of Allergy and Infectious Diseases; National Institutes of Health; Bethesda, MD 20189
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We agree with Baier-Bitterlich and colleagues that the mechanism by which interferon-γ acts in the setting of chronic infections such as leishmaniasis or tuberculosis is complex and may not fit neatly into the TH1/TH2 paradigm. Feedback loops, such as that which includes prostaglandin E2, are known to be down-regulatory for the destruction of intracellular pathogens at the macrophage level and are overcome by pharmacologic interferon-γ administration [1]. Similarly, interleukin-6 has been shown to down-regulate macrophage tumor necrosis factor-α receptor levels and to antagonize the interferon-γ-induced up-regulation of tumor necrosis factor-α receptor levels [2]. The general finding, however, has been that patients who progress to severe, disseminated infection with intracellular parasites such as Mycobacterium leprae or leishmania usually have abnormal lymphocyte proliferation and low interferon-γ production in response to antigen; these conditions return to normal after successful therapy [3, 4].
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Holland SM, Farber JM, Gallin JI. Interferon-γ and Management of Infectious Diseases. Ann Intern Med. 1996;124:1095–1096. doi: 10.7326/0003-4819-124-12-199606150-00016

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Published: Ann Intern Med. 1996;124(12):1095-1096.

DOI: 10.7326/0003-4819-124-12-199606150-00016

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Print ISSN: 0003-4819 | Online ISSN: 1539-3704

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