NDLI: Regulation of Human CD4+ αβT-Cell-Receptor-Positive (TCR+) and γδTCR+ T-Cell Responses to Mycobacteriumtuberculosis by Interleukin-10 and Transforming GrowthFactor β

Content Provider	PubMed Central
Author	Rojas, Roxana E. Balaji, Kithiganahalli N. Subramanian, Ahila Boom, W. Henry
Editor	Kaufmann, S. H. E.
Copyright Year	1999
Abstract	Mycobacterium tuberculosis is the etiologic agent ofhuman tuberculosis and is estimated to infect one-third of the world'spopulation. Control of M. tuberculosis requires T cells andmacrophages. 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 factoralpha) and inhibitory (IL-10 and transforming growth factor β[TGF-β]) cytokines. IL-10 and TGF-β are produced by M.tuberculosis-infected macrophages. The effect of IL-10 andTGF-β on M. tuberculosis-reactive human CD4+and γδ T cells, the two major human T-cell subsets activated byM. tuberculosis, was investigated. Both IL-10 and TGF-βinhibited proliferation and gamma interferon production byCD4+ and γδ T cells. IL-10 was a more potent inhibitorthan TGF-β for both T-cell subsets. Combinations of IL-10 and TGF-βdid not result in additive or synergistic inhibition. IL-10 inhibitedγδ and CD4+ T cells directly and inhibited monocyteantigen-presenting cell (APC) function for CD4+ T cellsand, to a lesser extent, for γδ T cells. TGF-β inhibited bothCD4+ and γδ T cells directly and had little effect onAPC function for γδ and CD4+ T cells. IL-10down-regulated major histocompatibility complex (MHC) class I, MHCclass II, CD40, B7-1, and B7-2 expression on M.tuberculosis-infected monocytes to a greater extent than TGF-β.Neither cytokine affected the uptake of M. tuberculosis bymonocytes. Thus, IL-10 and TGF-β both inhibited CD4+ andγδ T cells but differed in the mechanism used to inhibit T-cellresponses to M. tuberculosis.
Starting Page	6461
File Format	PDF
ISSN	10985522
e-ISSN	10985522
Journal	Infection and Immunity
Issue Number	12
Volume Number	67
Language	English
Publisher	American Society for Microbiology (ASM)
Publisher Date	1999-12-01
Access Restriction	Open
Rights Holder	American Society for Microbiology (ASM)
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Infectious Diseases Parasitology Immunology Microbiology

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