2023
DOI: 10.3389/fimmu.2023.1133394
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New pairings and deorphanization among the atypical chemokine receptor family — physiological and clinical relevance

Abstract: Atypical chemokine receptors (ACKRs) form a small subfamily of receptors (ACKR1–4) unable to trigger G protein-dependent signaling in response to their ligands. They do, however, play a crucial regulatory role in chemokine biology by capturing, scavenging or transporting chemokines, thereby regulating their availability and signaling through classical chemokine receptors. ACKRs add thus another layer of complexity to the intricate chemokine–receptor interaction network. Recently, targeted approaches and screen… Show more

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Cited by 14 publications
(11 citation statements)
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“…These atypical GPCRs all bind a variety of chemokines, but do not signal following the canonical G-protein pathways. In contrast, the ACKRs act as β-arrestin-biased GPCRs and are involved in the regulation of extracellular chemokine levels mostly via chemokine internalization and breakdown [14][15][16] .…”
Section: Introductionmentioning
confidence: 99%
“…These atypical GPCRs all bind a variety of chemokines, but do not signal following the canonical G-protein pathways. In contrast, the ACKRs act as β-arrestin-biased GPCRs and are involved in the regulation of extracellular chemokine levels mostly via chemokine internalization and breakdown [14][15][16] .…”
Section: Introductionmentioning
confidence: 99%
“…25,26 By acting as scavenger receptor, ACKR1 modulates the bioavailability of cytokines and thereby affects inflammatory responses. 27,28 The identified associations were driven by rs12075, a well-characterized missense variant in ACKR1, resulting in less efficient chemokine binding to ACKR1 due to loss of a necessary amino-acid sulfation ( Figure 6a ). 29 The impaired receptor binding leads to elevated circulatory levels of chemokines and might in turn result in a compensatory increase in ACKR1 expression which could explain the positive association between genetically proxied ACKR1 and its ligands.…”
Section: Resultsmentioning
confidence: 99%
“…GPR182 is primarily upregulated in melanoma-associated lymphatic endothelial cells during tumorigenesis and its knocking out increases T cell infiltration and improves antitumor immunity 5 . Similar to GPR182, the atypical chemokine receptor 2 (ACKR2) is involved in scavenging not only numerous CC chemokines but also CXCL10 chemokine 6,7 . Several chemokines associated with T cell-inflamed signatures, including CCL2, CCL4 and CCL5 and CXCL10 are scavenged by ACKR2 8 , and thus we postulated that targeting ACKR2 could be a valuable strategy to establish an inflamed TME susceptible to drive major cytotoxic immune cells and improve the benefit of anti-PD-1 immunotherapy.…”
Section: Short Reportmentioning
confidence: 99%