24
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Interleukin 27 negatively regulates the development of interleukin 17-producing T helper cells during chronic inflammation of the central nervous system.

      Nature immunology
      Animals, Antigens, CD4, analysis, Central Nervous System, immunology, parasitology, Encephalitis, pathology, Interleukin-17, Interleukin-6, genetics, metabolism, Interleukins, pharmacology, physiology, Lymphocyte Activation, Mice, Mice, Knockout, Receptors, Cytokine, drug effects, STAT1 Transcription Factor, Suppressor of Cytokine Signaling Proteins, T-Lymphocytes, Helper-Inducer, Toxoplasma, Toxoplasmosis, Cerebral

      Read this article at

      ScienceOpenPublisherPubMed
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Studies have focused on the events that influence the development of interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) associated with autoimmunity, such as experimental autoimmune encephalitis, but relatively little is known about the cytokines that antagonize T(H)-17 cell effector responses. Here we show that IL-27 receptor-deficient mice chronically infected with Toxoplasma gondii developed severe neuroinflammation that was CD4+ T cell dependent and was associated with a prominent IL-17 response. In vitro, treatment of naive primary T cells with IL-27 suppressed the development T(H)-17 cells induced by IL-6 and transforming growth factor-beta, which was dependent on the intracellular signaling molecule STAT1 but was independent of inhibition of IL-6 signaling mediated by the suppressor protein SOCS3. Thus IL-27, a potent inhibitor of T(H)-17 cell development, may be a useful target for treating inflammatory diseases mediated by these cells.

          Related collections

          Author and article information

          Comments

          Comment on this article