Research ArticleINFLAMMATION

Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation

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Science Immunology  10 May 2019:
Vol. 4, Issue 35, eaav5951
DOI: 10.1126/sciimmunol.aav5951

Atypical attraction

Neutrophils contribute to inflammatory responses by moving from the circulation into target tissues through a series of chemoattractant-driven steps involving arrest and transmigration. Here, Miyabe et al. use an immune complex–induced arthritis murine model to show that neutrophil arrest requires endothelial expression of the atypical complement C5a receptor 2 (C5aR2) to drive transport of C5a into the vessel lumen, which is required for initiation of C5aR1-driven neutrophil arrest. Expression of the atypical chemokine receptor 1 (ACKR1) on endothelial cells mediates transport of CXCR2 chemokine ligands into the lumen and CXCR2-dependent transendothelial migration of neutrophils. These results clarify a role for “atypical” chemoattractant receptors working in conjunction with classical chemoattractant receptors to drive neutrophil arrest and diapedesis.

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