The IL-27R (WSX-1) is required to suppress T cell hyperactivity during infection

Immunity. 2003 Nov;19(5):645-55. doi: 10.1016/s1074-7613(03)00300-5.


Although recent studies have described IL-27 and its receptor, WSX-1, as promoters of Th1 differentiation in naive CD4+ T cells, the data presented here indicate that signaling through this receptor is involved in limiting the intensity and duration of T cell activity. When WSX-1-deficient mice are infected with the intracellular pathogen Toxoplasma gondii, they establish protective T cell responses, characterized by production of inflammatory cytokines and control of parasite replication. However, infected WSX-1-/- mice are unable to downregulate these protective responses, and develop a lethal, T cell-mediated inflammatory disease. This pathology was characterized by the excessive production of IFN-gamma, persistence of highly activated T cells, and enhanced T cell proliferation in vivo. Together, these findings demonstrate that WSX-1 is not required for the generation of IFN-gamma-mediated immunity to this parasitic infection and identify a novel function for this receptor as a potent antagonist of T cell-mediated, immune hyperactivity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Differentiation / physiology
  • Infections / immunology*
  • Infections / metabolism
  • Mice
  • Mice, Knockout
  • Receptors, Cytokine / genetics
  • Receptors, Cytokine / metabolism*
  • Receptors, Interleukin
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*
  • Th1 Cells / physiology
  • Toxoplasma / immunology
  • Toxoplasmosis / immunology


  • Il27ra protein, mouse
  • Receptors, Cytokine
  • Receptors, Interleukin