Abstract
Atypical chemokine receptor 3 (ACKR3), previously known as C-X-C chemokine receptor type 7 (CXCR7), has emerged as a key player in several biologic processes, particularly during development. Its CXCL11 and CXCL12 scavenging activity and atypical signaling properties, together with a new array of other nonchemokine ligands, have established ACKR3 as a main regulator of physiologic processes at steady state and during inflammation. Here, we present a comprehensive review of ACKR3 expression in mammalian tissues in search of a possible connection with the receptor function. Besides the reported roles of ACKR3 during development, we discuss the potential contribution of ACKR3 to the function of the immune system, focusing on the myeloid lineage.
Footnotes
- Received December 14, 2018.
- Accepted April 24, 2019.
↵1 Current affiliation: Université de Paris, Institut de Recherche Saint Louis, EMiLy, Inserm U1160, F-75010 Paris, France.
↵2 J.K. and C.G. contributed equally to this work.
↵3 F.B., K.B., and G.S.-L. contributed equally to this work.
This mini-review is part of the mini-review series entitled “From Insight to Modulation of CXCR4 and ACKR3 (CXCR7) Function.” This research was funded by the European Union’s Horizon 2020 MSCA Program [Grant agreement 641833 ONCORNET] to all authors, by European Union’s Infect-ERA project HPV-Motiva [ANR-15-IFEC-0004-0] to F.B. and G.S.-L., and by a PRC ANR Grant OSTEOVALYMPH [17-CE14-0019] coordinated by K.B. All authors are members of the LabEx LERMIT supported by ANR grant [ANR-10-LABX-33] under the program “Investissements d’Avenir” [ANR-11-IDEX-0003-01]. C.G. is beneficiary of a fellowship from Fondation de la Recherche Medicale (FRM).
- Copyright © 2019 by The American Society for Pharmacology and Experimental Therapeutics
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