Online now: A CD4+ T cell-intrinsic complement C5aR2-prostacyclin-IL-1R2 axis orchestrates Th1 cell contraction
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The pathways regulating Th1 cell contraction are not well understood. Rahman et al. demonstrate that complement receptor C5aR2 controls T cell-intrinsic prostanoid metabolism as an integral component of Th1 cell contraction. Faulty C5aR2-prostanoid rewiring marks autoimmunity-associated hyper-Th1 cell responses in arthritis and Crohn’s disease. Therefore, prostanoid metabolism is a potentially druggable checkpoint for the cessation of Th1 cell effector responses.