ArticleFrontiers in immunology2023
GPR182 is a broadly scavenging atypical chemokine receptor influencing T-independent immunity.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Endothelial Atypical Receptors for Chemoattractants in Lung Immune Surveillance.European journal of immunology · 2026Review
- GPR182 and the reframing of lacteal chylomicron uptake.The Journal of clinical investigation · 2026Article
- GPR182 is a lipoprotein receptor for dietary fat absorption.The Journal of clinical investigation · 2026Article
- Atypical GPCR Activation Resolved by Nanobody Engineering.bioRxiv : the preprint server for biology · 2026Article
- Extended repertoire of CXC chemokines acting as agonists and antagonists of the human and murine atypical chemokine receptor ACKR2.Journal of leukocyte biology · 2025Article
- Inclusion of ACKR5 in the systematic nomenclature of atypical chemokine receptors.Nature reviews. Immunology · 2025Article
- Review
- Atypical chemokine receptors in the immune system.Nature reviews. Immunology · 2024Review
- Large chemokine binding spectrum of human and mouse atypical chemokine receptor GPR182 (ACKR5).Frontiers in pharmacology · 2023Article
- Chemokines, molecular drivers of thromboinflammation and immunothrombosis.Frontiers in immunology · 2023Review
- G protein-coupled receptor kinase 3 couples atypical chemokine receptor 4 independent of G proteins.Molecular pharmacologyArticle
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune responses highly depend on the effective trafficking of immune cells into and within secondary lymphoid organs (SLOs). Atypical chemokine receptors (ACKRs) scavenge chemokines to eliminate them from the extracellular space, thereby generating gradients that guide leukocytes. In contrast to canonical chemokine receptors, ACKRs do not induce classical intracellular signaling that results in cell migration. Recently, the closest relative of ACKR3, GPR182, has been partially deorphanized as a potential novel ACKR. We confirm and extend previous studies by identifying further ligands that classify GPR182 as a broadly scavenging chemokine receptor. We validate the "atypical" nature of the receptor, wherein canonical G-protein-dependent intracellular signaling is not activated following ligand stimulation. However, β-arrestins are required for ligand-independent internalization and chemokine scavenging whereas the C-terminus is in part dispensable. In the absence of GPR182
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.