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Interaction of Mycobacterium tuberculosis-induced transforming growth factor beta1 and interleukin-10

C Othieno1, C S Hirsch, B D Hamilton

  • 1Makerere University, Kampala, Uganda.

Infection and Immunity
|October 26, 1999
PubMed

Insights

Transforming growth factor beta1 (TGF-beta1) and interleukin-10 (IL-10) work together to suppress T-cell production of gamma interferon (IFN-gamma) in tuberculosis. TGF-beta1 also boosts IL-10, potentially hindering immune responses at infection sites.

Area of Science:

  • Immunology
  • Tuberculosis Research
  • Cytokine Signaling

Background:

  • Mycobacterium tuberculosis infection activates cytokine circuits in vivo and in vitro.
  • Cytokines interact through stimulatory and inhibitory pathways, modulating T-cell responses.
  • Understanding these interactions is crucial for controlling tuberculosis.

Purpose of the Study:

  • To investigate the interaction between transforming growth factor beta1 (TGF-beta1) and interleukin-10 (IL-10) in Mycobacterium tuberculosis-stimulated human mononuclear cells.
  • To determine how TGF-beta1 and IL-10 influence gamma interferon (IFN-gamma) production in T-cells.
  • To elucidate the role of these cytokine interactions in the context of active tuberculosis.

Main Methods:

  • Human mononuclear cell cultures stimulated with purified protein derivative (PPD) from M. tuberculosis.
  • Measurement of cytokine production (IL-10, TNF-alpha, IFN-gamma) and mRNA expression.
  • Use of exogenous recombinant TGF-beta1 and IL-10, and neutralization of endogenous cytokines.
  • Analysis of responses in peripheral blood mononuclear cells (PBMC) and monocyte-depleted cells.

Main Results:

  • TGF-beta1 induced significant monocyte IL-10 production, but not TNF-alpha, in the absence of PPD.
  • Both TGF-beta1 and IL-10 independently suppressed PPD-induced IFN-gamma production.
  • Synergistic suppression of IFN-gamma occurred when PBMC were pretreated with both TGF-beta1 and IL-10.
  • Neutralization of both TGF-beta1 and IL-10 synergistically enhanced PPD-induced IFN-gamma production.

Conclusions:

  • TGF-beta1 and IL-10 together potentiate the suppression of M. tuberculosis-induced T-cell IFN-gamma production.
  • TGF-beta1 enhances IL-10 production, contributing to immune suppression.
  • These cytokine interactions may suppress mononuclear cell function at sites of active tuberculosis.

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