| First Author | Villarino A | Year | 2003 |
| Journal | Immunity | Volume | 19 |
| Issue | 5 | Pages | 645-55 |
| PubMed ID | 14614852 | Mgi Jnum | J:309520 |
| Mgi Id | MGI:6758296 | Doi | 10.1016/s1074-7613(03)00300-5 |
| Citation | Villarino A, et al. (2003) The IL-27R (WSX-1) is required to suppress T cell hyperactivity during infection. Immunity 19(5):645-55 |
| abstractText | 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. |
