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Updated: Jun 13, 2025

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
Published on: September 15, 2017
A backhanded complement: Prostacyclin turns inflammation off from the inside out
Samuel E J Preston1, Russell G Jones1
1Department of Metabolism and Nutritional Programming, Van Andel Institute, Grand Rapids, MI, USA.
To limit hyperactive T helper (Th)1-driven pathology, it is crucial that this T cell population contracts upon pathogen clearance. In this issue of Immunity, Rahman et al. define a complement-C5-mediated lipid-class-switch mechanism that regulates Th1 self-control. Following activation, enhanced cell-intrinsic prostacyclin (PGI2) signaling boosts interleukin (IL)-1R2 production to facilitate Th1 cell contraction.
To limit hyperactive T helper (Th)1-driven pathology, it is crucial that this T cell population contracts upon pathogen clearance. In this issue of Immunity, Rahman et al. define a complement-C5-mediated lipid-class-switch mechanism that regulates Th1 self-control. Following activation, enhanced cell-intrinsic prostacyclin (PGI2) signaling boosts interleukin (IL)-1R2 production to facilitate Th1 cell contraction.
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