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Research Article Free access | 10.1172/JCI117031

Role of interleukin-10 in T helper cell dysfunction in asymptomatic individuals infected with the human immunodeficiency virus.

M Clerici, T A Wynn, J A Berzofsky, S P Blatt, C W Hendrix, A Sher, R L Coffman, 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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Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

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Published February 1, 1994 - More info

Published in Volume 93, Issue 2 on February 1, 1994
J Clin Invest. 1994;93(2):768–775. https://doi.org/10.1172/JCI117031.
© 1994 The American Society for Clinical Investigation
Published February 1, 1994 - Version history
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Abstract

The loss of T helper cell (TH) function in asymptomatic HIV type 1-infected individuals occurs before the decline in CD4+ T cells. At least part of the loss in TH function results from changes in immunoregulatory cytokine profiles. To investigate the role of IL-10 in such dysregulation, we tested whether: (a) expression of IL-10-specific mRNA would be upregulated in PBMC from asymptomatic, HIV-infected (HIV+) individuals; (b) PBMC from these same individuals would produce increased levels of IL-10 when stimulated in vitro with phytohemagglutinin; and (c) defective antigen-specific TH function could be restored by anti-IL-10 antibody. We observed that IL-10-specific mRNA was marginally upregulated, and increased levels of IL-10 were produced by PBMC from HIV+ individuals compared with PBMC from uninfected individuals. Those individuals whose TH function was more severely compromised produced higher levels of IL-10. Additionally, defective antigen-specific TH function in vitro could be reversed by anti-IL-10 antibody, including the response to HIV envelope synthetic peptides. Furthermore, the antigen-specific TH responses of HIV-uninfected PBMC could be reduced with IL-10, a process reversed by anti-IL-10. These results confirm that the early loss of TH function in HIV+ individuals is due at least in part to cytokine-induced immune dysregulation, and support the hypothesis of a switch from a predominant type 1 state to a predominant type 2 condition in HIV infection.

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