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Infection and Immunity, December 1999, p. 6461-6472, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Regulation of Human CD4+ alpha beta T-Cell-Receptor-Positive (TCR+) and gamma delta TCR+ T-Cell Responses to Mycobacterium tuberculosis by Interleukin-10 and Transforming Growth Factor beta

Roxana E. Rojas, Kithiganahalli N. Balaji,dagger Ahila Subramanian, and W. Henry Boom*

Department of Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106-4984

Received 12 May 1999/Returned for modification 15 June 1999/Accepted 15 September 1999

Mycobacterium tuberculosis is the etiologic agent of human tuberculosis and is estimated to infect one-third of the world's population. Control of M. tuberculosis requires T cells and macrophages. T-cell function is modulated by the cytokine environment, which in mycobacterial infection is a balance of proinflammatory (interleukin-1 [IL-1], IL-6, IL-8, IL-12, and tumor necrosis factor alpha) and inhibitory (IL-10 and transforming growth factor beta  [TGF-beta ]) cytokines. IL-10 and TGF-beta are produced by M. tuberculosis-infected macrophages. The effect of IL-10 and TGF-beta on M. tuberculosis-reactive human CD4+ and gamma delta T cells, the two major human T-cell subsets activated by M. tuberculosis, was investigated. Both IL-10 and TGF-beta inhibited proliferation and gamma interferon production by CD4+ and gamma delta T cells. IL-10 was a more potent inhibitor than TGF-beta for both T-cell subsets. Combinations of IL-10 and TGF-beta did not result in additive or synergistic inhibition. IL-10 inhibited gamma delta and CD4+ T cells directly and inhibited monocyte antigen-presenting cell (APC) function for CD4+ T cells and, to a lesser extent, for gamma delta T cells. TGF-beta inhibited both CD4+ and gamma delta T cells directly and had little effect on APC function for gamma delta and CD4+ T cells. IL-10 down-regulated major histocompatibility complex (MHC) class I, MHC class II, CD40, B7-1, and B7-2 expression on M. tuberculosis-infected monocytes to a greater extent than TGF-beta . Neither cytokine affected the uptake of M. tuberculosis by monocytes. Thus, IL-10 and TGF-beta both inhibited CD4+ and gamma delta T cells but differed in the mechanism used to inhibit T-cell responses to M. tuberculosis.

* Corresponding author. Mailing address: Division of Infectious Diseases, Case Western Reserve University, School of Medicine, BRB 10th Floor, 10900 Euclid Ave., Cleveland, OH 44106-4984. Phone: (216) 368-4844. Fax: (216) 368-2034. E-mail: whb{at}po.cwru.edu.

dagger Present address: Lymphocyte Cytotoxicity Section, Experimental Immunology Branch, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1360.

Infection and Immunity, December 1999, p. 6461-6472, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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