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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Intern Med. 2017 May 31;282(1):76–93. doi: 10.1111/joim.12619

Figure 8. Model of haptoglobin β subunit as an endogenous inhibitor of HMGB1.

Figure 8

During infection or injury, HMGB1, a critical mediator in the final common pathway of inflammation, is actively secreted or passively released outside of the cells. Haptoglobin binds HMGB1 and inhibits its toxicity; and haptoglobin β subunit alone is sufficient to recapitulate the effects of the full-length haptoglobin. HMGB1-haptoglobin β complexes act via CD163 and elicit an anti-inflammatory response by stimulating HO-1 expression and IL-10 release; and by inhibiting pro-inflammatory cytokine release. Thus, haptoglobin β acts as an endogenous inhibitor of HMGB1 via a novel CD163-dependent anti-inflammatory pathway.