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Research Article Free access | 10.1172/JCI117611

T cell cytokine responses in persons with tuberculosis and human immunodeficiency virus infection.

M Zhang, J Gong, D V Iyer, B E Jones, R L Modlin, and P F Barnes

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Zhang, M. in: PubMed | Google Scholar

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Gong, J. in: PubMed | Google Scholar

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Iyer, D. in: PubMed | Google Scholar

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Jones, B. in: PubMed | Google Scholar

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Modlin, R. in: PubMed | Google Scholar

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Find articles by Barnes, P. in: PubMed | Google Scholar

Published December 1, 1994 - More info

Published in Volume 94, Issue 6 on December 1, 1994
J Clin Invest. 1994;94(6):2435–2442. https://doi.org/10.1172/JCI117611.
© 1994 The American Society for Clinical Investigation
Published December 1, 1994 - Version history
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Abstract

Tuberculosis causes more extensive and life-threatening disease in patients with HIV infection than in immunocompetent persons. To investigate the hypothesis that these severe manifestations of tuberculosis may be due to alterations in cytokine production, we evaluated cytokine patterns in HIV-infected tuberculosis patients. Upon stimulation with Mycobacterium tuberculosis in vitro, PBMC from HIV-infected tuberculosis patients had reduced proliferative and type 1 responses, compared with HIV-seronegative tuberculosis patients. The reduction in proliferative responses was independent of the CD4 cell count, but the reduced type 1 response was a direct result of CD4 cell depletion. There was no enhancement of type 2 cytokine production in HIV-infected patients, although production of IL-10 was prominent in all tuberculosis patients. In HIV-infected tuberculosis patients, M. tuberculosis-induced proliferative responses were significantly enhanced by neutralizing antibodies to IL-10 but not by antibodies to IL-4 or by recombinant IL-12. The M. tuberculosis-induced type 1 response was augmented both by antibodies to IL-10 and by recombinant IL-12. Tuberculosis in the context of HIV infection is characterized by diminished type 1 responses, probably induced by immunosuppressive cytokines produced by macrophages/monocytes, rather than by type 2 cells.

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