Journal
IMMUNITY
Volume 19, Issue 5, Pages 645-655Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(03)00300-5
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- PHS HHS [41158] Funding Source: Medline
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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 INSX-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.
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