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Research Article Free access | 10.1172/JCI116294

Changes in interleukin-2 and interleukin-4 production in asymptomatic, human immunodeficiency virus-seropositive individuals.

M Clerici, F T Hakim, D J Venzon, S Blatt, C W Hendrix, T A Wynn, and G M Shearer

Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Published March 1, 1993 - More info

Published in Volume 91, Issue 3 on March 1, 1993
J Clin Invest. 1993;91(3):759–765. https://doi.org/10.1172/JCI116294.
© 1993 The American Society for Clinical Investigation
Published March 1, 1993 - Version history
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Abstract

Infection with HIV results in an incremental loss of T helper cell (TH) function, which can occur years before CD4 cell numbers are critically reduced and AIDS is diagnosed. All TH function is not affected, however, because B cell activation and hypergammaglobulinema are also characteristic of this period. Recently, in a murine model of AIDS an early loss in production of the CD4 cytokines IL-2 and IFN-gamma was correlated with an increase in the B cell stimulatory cytokines IL-4, IL-5, and IL-10. We therefore assessed the production of IL-4 generated by PBL from HIV-seropositive (HIV+) individuals who did not have AIDS, yet who exhibited different TH functional categories based on their IL-2 production profiles. We observed that the decreases in recall antigen-stimulated IL-2 production were accompanied by an increase in IL-4 production. The loss of recall antigen-stimulated responses in HIV+ individuals could be reversed in vitro by anti-IL-4 antibody. Our results suggest that the TH functions assessed by IL-4 production replace the normally dominant TH function of antigen-stimulated IL-2 production in the progression toward AIDS, and raise the possibility of cytokine cross-regulation in AIDS therapy.

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