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Regulation Of Human CD4(+) Alphabeta T-cell-receptor-positive (TCR(+)) And Gammadelta TCR(+) T-cell Responses To Mycobacterium Tuberculosis By Interleukin-10 And Transforming Growth Factor Beta.
| Content Provider | Indian Institute of Science (IISc) |
|---|---|
| Author | Rojas, R. E. Balaji, K. N. Subramanian, A. Boom, W. H. |
| Copyright Year | 1999 |
| Abstract | 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 gammadelta 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 gammadelta 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 gammadelta and CD4(+) T cells directly and inhibited monocyte antigen-presenting cell (APC) function for CD4(+) T cells and, to a lesser extent, for gammadelta T cells. TGF-beta inhibited both CD4(+) and gammadelta T cells directly and had little effect on APC function for gammadelta 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 gammadelta T cells but differed in the mechanism used to inhibit T-cell responses to M. tuberculosis. |
| File Format | |
| Journal | PeerReviewed |
| Language | English |
| Publisher | American Society for Microbiology |
| Publisher Date | 1999-12-01 |
| Access Restriction | Authorized |
| Subject Keyword | Microbiology & Cell Biology |
| Content Type | Text |
| Resource Type | Article |
