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. 2016 Aug 22;213(9):1655–1662. doi: 10.1084/jem.20160061

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© 2016 Littlewood-Evans et al.

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Figure 4. — Proposed mechanism of GPR91-driven autocrine and paracrine enhancement of IL-1β release from activated macrophages. Endogenous TLR ligands in the SF of RA patients activate macrophages locally. This leads to an enhancement of glycolysis and an increase of intracellular succinate. At the same time, succinate is released to the extracellular milieu where it binds to GPR91 and amplifies IL-1β production from either the same or a neighboring GPR91-expressing cell. Both LPS and IL-1β up-regulate GPR91 in a further feed-forward action to perpetuate inflammation.

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