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Related Experiment Videos

IL-27 limits IL-2 production during Th1 differentiation.

Alejandro V Villarino1, Jason S Stumhofer, Christiaan J M Saris

  • 1Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 21, 2005
PubMed
Summary

Interleukin-27 (IL-27) limits harmful T cell responses by suppressing Interleukin-2 (IL-2) production, preventing lethal inflammation during Toxoplasma gondii infection. This reveals a key anti-inflammatory role for IL-27.

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Area of Science:

  • Immunology
  • Cytokine Biology
  • Infectious Disease

Background:

  • The anti-inflammatory functions of Interleukin-27 (IL-27) are not well understood, despite its known role in promoting T cell responses.
  • Toxoplasma gondii infection in mice lacking the IL-27 receptor (IL-27R) leads to severe inflammatory disease and aberrant IL-2 production.

Purpose of the Study:

  • To investigate the anti-inflammatory mechanisms of IL-27 during infection.
  • To determine how IL-27 regulates IL-2 production and its impact on immunopathology.

Main Methods:

  • Utilizing IL-27R-deficient mice infected with Toxoplasma gondii.
  • Analyzing IL-2 production in CD4+ T cells in vitro and in vivo.
  • Investigating the effects of recombinant IL-27 (rIL-27) and IL-12 on IL-2 expression.

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  • Examining the role of Suppressor of Cytokine Signaling 3 (SOCS3).

    • Main Results:

    • IL-27R-deficient mice exhibited lethal inflammatory disease driven by excessive IL-2 responses.
    • Depletion of IL-2 in these mice improved survival, indicating IL-2's pathogenic role.
    • IL-27 directly suppressed IL-2 mRNA and protein production by T cells.
    • Both IL-27 and IL-12 inhibited IL-2 production, acting synergistically and inducing SOCS3.

    Conclusions:

    • IL-27 acts as an anti-inflammatory cytokine by limiting IL-2 production, thereby preventing severe immunopathology.
    • IL-27 and IL-12 share inhibitory properties, including the induction of SOCS3, to temper T cell responses.
    • These findings redefine IL-27 and IL-12 as crucial regulators of T cell proliferation and inflammation.