Affinage

C5AR2

C5a anaphylatoxin chemotactic receptor 2 · UniProt Q9P296

Length
337 aa
Mass
36.1 kDa
Annotated
2026-04-28
99 papers in source corpus 37 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

C5AR2 (also called C5L2/GPR77) is an atypical seven-transmembrane complement receptor that binds C5a and C5a desArg with high affinity but is uncoupled from heterotrimeric G proteins due to a leucine substitution in its DRY motif, instead signaling through β-arrestin recruitment and clathrin-dependent internalization (PMID:12899627, PMID:19100624, PMID:19641221). C5AR2 functions as a context-dependent immunomodulator: in neutrophils and macrophages it predominantly restrains C5aR1-mediated pro-inflammatory signaling—suppressing ERK phosphorylation, chemotaxis, and cytokine production via β-arrestin pathway competition and physical heterodimerization with C5aR1—while in other settings it positively facilitates C5aR1 internalization, promotes NLRP3 inflammasome activation and HMGB1 release through PKR/MEK/IFN-I signaling, negatively regulates the cGAS-STING-IFN-β axis, and on endothelial cells transcytoses C5a to initiate neutrophil arrest (PMID:20044484, PMID:30971430, PMID:31076525, PMID:38067135, PMID:24631530). Beyond immunity, C5AR2 serves as the functional receptor for acylation-stimulating protein (C3a desArg), mediating triglyceride synthesis and glucose transport in adipocytes through serine 323-dependent β-arrestin signaling, and on CD4+ T cells it orchestrates Th1 contraction via a prostacyclin–IL-1R2 axis whose disruption characterizes pathological Th1 persistence in autoinflammatory diseases (PMID:15833747, PMID:19615750, PMID:40449486).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2001 High

    Identification of C5L2 as a high-affinity C5a/C5a desArg receptor that does not trigger classical GPCR effector responses (degranulation, Ca²⁺ flux) established it as an atypical complement receptor with undefined signaling capacity.

    Evidence Radioligand binding, Ca²⁺ flux, and degranulation assays in C5L2-transfected RBL-2H3 cells

    PMID:11773063

    Open questions at the time
    • Signaling mechanism downstream of ligand binding undefined
    • Physiological role in primary cells unknown
  2. 2003 High

    Demonstration that C5L2 is obligately G-protein-uncoupled due to the DRY→DLC motif substitution, with no MAPK, Ca²⁺, or chemotactic activity, raised the question of whether it functions as a signaling receptor or a decoy/scavenger.

    Evidence Multi-cell-line transfection with G-protein coupling, MAPK, and chemotaxis assays; C5aR-deficient mouse microarray showing no transcriptional response via C5L2 alone

    PMID:12899627

    Open questions at the time
    • Mechanism by which C5L2 modulates C5a biology without G-protein coupling unknown
    • Potential non-G-protein signaling not yet explored
  3. 2005 High

    Gain- and loss-of-function experiments established C5L2 as a functional receptor for ASP/C3a desArg that drives triglyceride synthesis via β-arrestin recruitment, revealing the first signaling pathway for this receptor; simultaneously, C5L2-knockout mice showed enhanced C5a responses, defining C5L2 as an anti-inflammatory modulator in vivo.

    Evidence Stable transfection and antisense knockdown in fibroblasts/adipocytes with TG synthesis, glucose transport, β-arrestin-GFP translocation; C5L2 KO mice challenged with C5a in vivo; anti-C5L2 antibody blockade in rat sepsis model

    PMID:15784721 PMID:15833747 PMID:16204243

    Open questions at the time
    • Whether anti-inflammatory and metabolic functions use the same or distinct β-arrestin pathways unclear
    • Binding of C3a/C3a desArg disputed by subsequent study
  4. 2007 High

    Paradoxically, an independent C5L2 KO study found C5L2 facilitates (rather than suppresses) C5a signaling in neutrophils and macrophages, and C5L2 KO mice paralleled C3aR KO phenotypes in asthma and sepsis models, revealing the first evidence that C5L2's net effect is context-dependent.

    Evidence Gene-targeted C5L2 KO mice in LPS sepsis, OVA airway, and irradiation models; in vitro C5a signaling in multiple primary cell types

    PMID:17322907

    Open questions at the time
    • Molecular basis for discrepancy with earlier KO study unresolved
    • Cell-type-specific roles not yet dissected
  5. 2008 High

    Discovery that C5L2 is predominantly intracellular in neutrophils, co-localizes with internalized C5aR and β-arrestin, and that its blockade selectively enhances ERK but not Ca²⁺ signaling established the β-arrestin pathway competition model for C5L2's anti-inflammatory activity; separately, C5L2 was shown to constitutively internalize and degrade C5a via clathrin-dependent endocytosis, defining its decoy/scavenging function.

    Evidence Confocal microscopy, Co-IP of C5L2–β-arrestin, antibody blockade with ERK/Ca²⁺ readouts in human neutrophils; clathrin dominant-negative inhibition and ligand degradation tracking in transfected cells

    PMID:19100624 PMID:20044484

    Open questions at the time
    • Structural basis for β-arrestin recruitment without G-protein coupling unknown
    • Relative contributions of decoy versus signaling functions unquantified
  6. 2009 High

    Detailed trafficking analysis showed C5L2 undergoes ligand-dependent clathrin/cholesterol-dependent endocytosis through Rab5→Rab7→Rab11 compartments, and serine 323 is essential for surface localization, phosphorylation, β-arrestin-2 recruitment, and all downstream metabolic functions.

    Evidence Rab-GFP co-localization, S323I mutagenesis with β-arrestin-2 translocation and TG synthesis assays in stably transfected HEK cells; β-galactosidase complementation confirming direct C5L2–β-arrestin interaction

    PMID:19615750 PMID:19641221

    Open questions at the time
    • Whether S323 phosphorylation is mediated by GRKs or other kinases unknown
    • Crystal/cryo-EM structure of C5L2 absent
  7. 2012 Medium

    BRET experiments demonstrated constitutive C5aR-C5L2 homo- and heterodimer formation, with C5a-induced upregulation of heteromers, providing a physical basis for functional crosstalk between the two receptors.

    Evidence BRET in transfected HEK293 cells; confocal co-localization in 3T3-L1 adipocytes and J774 macrophages

    PMID:23268185 PMID:24060963

    Open questions at the time
    • Heterodimer stoichiometry and structural interface undefined
    • BRET proximity does not prove functional requirement for dimerization in all contexts
    • In vivo confirmation of heterodimerization lacking
  8. 2013 High

    Epistatic studies in allergic contact dermatitis and sepsis models showed C5L2's anti-inflammatory effect is reversed by C5aR1 blockade, while C5L2 and C5aR1 are both required for optimal G-CSF production, demonstrating that C5L2 both restrains and cooperates with C5aR1 depending on downstream pathway.

    Evidence C5L2 KO mice with anti-C5aR mAb rescue in contact sensitivity; dual C5aR1/C5L2 KO macrophages with PI3K/MEK inhibitors in CLP sepsis

    PMID:23575697 PMID:24043888

    Open questions at the time
    • Molecular determinants that switch C5L2 from inhibitory to cooperative mode unknown
  9. 2014 High

    C5L2 was found to physically interact with C5aR and be required for AP2-dependent C5aR internalization and downstream MEK/ERK signaling, defining a positive facilitatory mechanism for C5aR endocytosis.

    Evidence Co-IP, dynasore inhibition, AP2 recruitment assay, ERK phosphorylation in transfected cells; C5L2 KO mice in acute colitis

    PMID:24631530

    Open questions at the time
    • Whether AP2 recruitment requires direct C5L2–AP2 contact or an adaptor protein unknown
  10. 2015 High

    In LAD2 mast cells expressing C5aR2 but not C5aR1, C5a independently drove ERK phosphorylation, cytokine production, and chemotaxis via β-arrestin-2/PI3K, proving C5aR2 can signal autonomously without C5aR1.

    Evidence Lentiviral shRNA knockdown of C5aR2, β-arrestin-2 siRNA, PI3K inhibitor in LAD2 cells with multiple functional readouts

    PMID:26283482

    Open questions at the time
    • Generalizability to other cell types expressing only C5aR2 not tested
    • Downstream transcription factor targets of autonomous C5aR2 signaling unknown
  11. 2017 High

    A genetic reporter mouse mapped C5aR2 expression across immune lineages (strong in neutrophils, myeloid cells, NK cells; absent from T cells), and functional validation showed C5aR2 ligation suppresses C5a-driven ERK in neutrophils and IL-12/IL-18-induced IFN-γ in NK cells, defining cell-type-specific anti-inflammatory functions.

    Evidence Floxed tdTomato-C5aR2 knock-in reporter mouse with flow cytometry; ERK assays in neutrophils; IFN-γ assay in NK cells

    PMID:28864475

    Open questions at the time
    • Expression and function in non-hematopoietic lineages (e.g. neurons, fibroblasts) not fully addressed by reporter
  12. 2018 High

    CD10⁺GPR77⁺ cancer-associated fibroblasts were shown to sustain cancer stemness via C5aR2-driven NF-κB activation, with neutralizing anti-GPR77 antibody abolishing tumor formation and restoring chemosensitivity, establishing a pro-tumorigenic role for C5aR2 in the tumor microenvironment.

    Evidence Patient-derived xenografts, anti-GPR77 neutralizing antibody, NF-κB reporter and p65 phosphorylation/acetylation assays

    PMID:29395328

    Open questions at the time
    • Ligand driving C5aR2 on CAFs in vivo not definitively identified
    • Whether NF-κB activation uses β-arrestin or an alternative adaptor unknown
  13. 2019 High

    C5aR2 on endothelial cells was identified as a transcytotic transporter that shuttles C5a from perivascular tissue to the vascular lumen to initiate C5aR1-dependent neutrophil arrest, establishing a non-signaling transport function for C5aR2 analogous to atypical chemokine receptors.

    Evidence Intravital microscopy in C5aR2 KO and ACKR1 KO mice in immune complex arthritis model

    PMID:31076525

    Open questions at the time
    • Molecular machinery of C5aR2-mediated transcytosis (vesicular carriers, sorting signals) undefined
    • Whether transcytosis is bidirectional unknown
  14. 2019 High

    C5aR2 was shown to promote NLRP3 inflammasome activation and HMGB1 release from macrophages by upregulating PKR expression through MEK/ERK and type I IFN signaling, with HMGB1 acting upstream of NLRP3 in this pathway, defining a pro-inflammatory signaling cascade distinct from the anti-inflammatory β-arrestin competition model.

    Evidence C5aR2 KO macrophages, siRNA, MEK inhibitor, HMGB1 blocking antibody; validated in acute pyelonephritis model

    PMID:30971430 PMID:32191644

    Open questions at the time
    • How C5aR2 activates MEK/ERK for PKR induction without G-protein coupling is mechanistically unresolved
    • Whether this pathway operates in non-macrophage cell types unknown
  15. 2020 High

    Selective C5aR2 agonism broadly dampened signaling from multiple innate receptors (C5aR1, C3aR, CMKLR1, TLR2/3/4/7, Dectin-1/2, Mincle, STING), reducing cytokine output by up to 90%, establishing C5aR2 as a global negative regulator of innate immune receptor signaling.

    Evidence Selective C5aR2 agonist P32 in primary human monocyte-derived macrophages with ERK, Ca²⁺, and multi-cytokine readouts across diverse PRR stimulations; validated with C5aR2 KO mice

    PMID:27108698 PMID:32611725

    Open questions at the time
    • Molecular mechanism by which C5aR2 cross-inhibits unrelated PRR pathways not defined
    • Whether tonic C5aR2 signaling operates without exogenous ligand unknown
  16. 2022 High

    Conditional (LysM-Cre) C5aR2 deletion showed that myeloid-intrinsic C5aR2 is required for full neutrophil effector function (Ca²⁺ flux, ROS, migration) and modulates activating/inhibitory FcγR ratios, demonstrating a cell-autonomous role in tuning neutrophil responsiveness.

    Evidence LysM-Cre/C5aR2-flox conditional KO and global KO mice in EBA model; in vitro Ca²⁺, ROS, migration, and FcγR flow cytometry

    PMID:35007559

    Open questions at the time
    • Mechanism linking C5aR2 to FcγR expression not elucidated
    • Whether myeloid-specific deletion fully recapitulates global KO in all disease models untested
  17. 2023 High

    CRISPR knockout of C5aR2 in macrophages upregulated STING and IRF3 expression and enhanced IFN-β secretion, with transcriptomics revealing de-repression of nucleic acid sensing pathways, establishing C5aR2 as a tonic negative regulator of the cGAS-STING-IFN-β axis.

    Evidence CRISPR-Cas9 KO in THP-1 and primary human monocyte-derived macrophages; IFN-β ELISA, STING/IRF3 Western blot, RNA-seq

    PMID:38067135

    Open questions at the time
    • Whether C5aR2 suppresses STING transcriptionally or post-translationally unclear
    • Ligand dependence of tonic STING suppression not determined
  18. 2025 High

    C5aR2 on CD4⁺ T cells was found to orchestrate Th1 contraction through a C5a→C5aR2→PGI₂→IL-1R2 axis that sequesters Th1-promoting IL-1β, with disruption of this pathway linked to pathological Th1 persistence in CAPS, Crohn's disease, and rheumatoid arthritis.

    Evidence T cell-intrinsic genetic/pharmacological dissection, prostaglandin profiling, IL-1R2 expression assay; validated in human CAPS patient T cells treated with PGE2 synthase inhibitor

    PMID:40449486

    Open questions at the time
    • Whether C5aR2 expression on T cells is context-inducible or constitutive across T cell subsets unclear
    • Source of C5a driving this axis in vivo not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for C5aR2's selective β-arrestin coupling without G-protein engagement; the molecular mechanism by which C5aR2 cross-inhibits diverse unrelated innate receptors (TLRs, STING, Dectins); and the determinants that switch C5aR2 between pro-inflammatory (NLRP3/NF-κB) and anti-inflammatory (ERK suppression/decoy) modes in different cell types.
  • No high-resolution structure of C5aR2 or C5aR2–β-arrestin complex
  • Mechanism of cross-receptor inhibition undefined
  • No unified model reconciling pro- and anti-inflammatory functions across cell types

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 10 GO:0060089 molecular transducer activity 5 GO:0038024 cargo receptor activity 2 GO:0140104 molecular carrier activity 1
Localization
GO:0005886 plasma membrane 4 GO:0031410 cytoplasmic vesicle 3 GO:0005768 endosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-168256 Immune System 18 R-HSA-162582 Signal Transduction 8 R-HSA-1430728 Metabolism 3 R-HSA-1643685 Disease 2 R-HSA-5357801 Programmed Cell Death 2
Partners
AP2ARRB2C5C5AR1EIF2AK2NLRP3
Complex memberships
C5aR1-C5aR2 heterodimer

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 C5L2 (C5AR2) binds C5a with high affinity and has ~10-fold higher affinity for C5a des-Arg74 than CD88/C5aR; it also binds C3a at a distinct site. Unlike CD88, C5L2 does not support degranulation or intracellular Ca2+ increases and is not rapidly internalized, but ligation potentiated IgE receptor-mediated degranulation via a pertussis toxin-sensitive mechanism. Radioligand binding assays, degranulation assays, Ca2+ flux assays in RBL-2H3 cells transfected with C5L2 The Journal of biological chemistry High 11773063
2003 C5L2 is obligately uncoupled from heterotrimeric G proteins due to a leucine-for-arginine substitution in the DRY motif (end of TM3); it does not induce MAP kinase activation, calcium flux, or chemotaxis following C5a binding. C5L2 has slow ligand on/off rates and does not internalize following C5a binding. Transfection of human and murine C5L2 into multiple cell lines, G protein coupling assays, MAP kinase assays, Ca2+ flux, chemotaxis, radiolabeled ligand binding kinetics; C5aR-deficient mice bearing only C5L2 showed no transcriptional response to C5a by microarray Biochemistry High 12899627
2003 C5L2 binds C3a des-Arg77/acylation-stimulating protein (ASP) at a site distinct from the C5a binding site; C5L2 mRNA and protein are expressed in human skin fibroblasts and adipocytes, which are ASP-responsive cells. Radioligand binding, cross-competition assays, RT-PCR, Western blot in human skin fibroblasts and 3T3-L1 cells The Journal of biological chemistry Medium 12540846
2005 C5L2 is a functional receptor for acylation-stimulating protein (ASP/C3a des-Arg): stable transfection of C5L2 into HEK293 cells confers ASP-stimulated triglyceride synthesis and glucose transport; antisense knockdown of C5L2 abolishes ASP response; ASP induces beta-arrestin translocation and C5L2 phosphorylation. Stable transfection, antisense oligonucleotide knockdown, triglyceride synthesis assay, glucose transport assay, DAPI-DAGL enzyme activity, beta-arrestin-GFP translocation, receptor phosphorylation in human skin fibroblasts and 3T3-L1 cells The Journal of biological chemistry High 15833747
2005 Targeted deletion of C5L2 in mice enhances the biological activity of C5a/C5a desArg both in vivo and in vitro, demonstrating that C5L2 functions as a negative (anti-inflammatory) modulator limiting the pro-inflammatory response to C5a. C5L2 knockout mice; in vivo C5a challenge; in vitro functional assays with C5L2-deficient cells The Journal of biological chemistry High 16204243
2005 C5L2 in rat neutrophils (PMN) during sepsis increases over time following CLP, while C5aR decreases; in vitro, C5a (but not fMLP) reduces C5L2 levels on PMN; anti-C5L2 antibody treatment causes ~4-fold increase in IL-6 during sepsis, indicating C5L2 negatively modulates C5a-driven IL-6 production. Rat CLP sepsis model, cloning of rat C5L2, anti-C5L2 antibody blockade in vivo and in vitro, ELISA for IL-6 FASEB journal Medium 15784721
2006 The N-terminal domain of C5L2 contains critical acidic and tyrosine residues for binding C5a des-Arg but not intact C5a; an antibody against the N-terminus of human C5L2 inhibited C5a des-Arg binding but not C5a binding, revealing that C5L2 binds C5a and C5a des-Arg by distinct mechanisms. Antibody blockade of chimeric/mutant C5L2 receptors, radioligand binding assays, mutagenesis of N-terminal residues The Journal of biological chemistry High 17158873
2006 C5L2 does not bind C3a or C3a des-Arg77 (ASP), as demonstrated by 125I-ligand binding assays with fluorescently labeled ligands on transfected HEK293 and myeloblastic cell lines, contradicting earlier reports; C5L2 expression on myeloid lines is upregulated by dibutyryl-cAMP and IFN-γ but downregulated by TNF-α on HeLa cells; no C5a-dependent Ca2+ signaling detected from endogenously expressing HeLa cells. 125I-ligand binding assays, flow cytometry with fluorescent ligands, quantitative real-time PCR, Ca2+ flux assay The Journal of biological chemistry Medium 17068344
2007 C5L2 gene-targeted mice demonstrate that C5L2 is required to facilitate C5a signaling (positive modulator) in neutrophils, macrophages, and fibroblasts in vitro; C5L2 deficiency reduces inflammatory cell infiltration in vivo; C5L2-deficient mice are hypersensitive to LPS-induced septic shock, show reduced OVA-induced airway inflammation, and are mildly delayed in hematopoietic regeneration after irradiation — paralleling C3aR-deficient phenotypes. Gene targeting (KO mice), in vitro C5a signaling assays in multiple cell types, in vivo models: LPS sepsis, OVA airway challenge, gamma-irradiation Nature High 17322907
2007 C5L2 KO mice on high-fat diet have significantly reduced adipose tissue triglyceride synthesis, lipolysis, and fatty acid re-esterification, with compensatory increases in muscle fatty acid oxidation (elevated UCP3, CD36, cytochrome c, phospho-ACC in skeletal muscle). C5L2 KO mice, adipose tissue TG synthesis assay, lipolysis assay, indirect calorimetry, Western blotting of muscle metabolic proteins The Journal of endocrinology High 17641279
2008 Human C5L2 is predominantly intracellular in neutrophils (versus C5aR at the plasma membrane); C5L2 co-localizes with internalized C5aR and beta-arrestin; antibody blockade of C5L2 dramatically increases C5a-mediated chemotaxis and ERK1/2 phosphorylation but not Ca2+ mobilization; C5L2 associates with beta-arrestin by co-immunoprecipitation; C5L2 blockade does not affect C5aR endocytosis — establishing C5L2 as a negative modulator of C5aR signaling through the beta-arrestin pathway. Confocal microscopy, antibody blockade, chemotaxis assay, ERK1/2 phosphorylation assay, Ca2+ mobilization, co-immunoprecipitation in human neutrophils/PMNs The Journal of biological chemistry High 20044484
2008 Human C5L2 constitutively internalizes ligand via clathrin-dependent endocytosis independently of G-protein coupling; internalized ligand is retained and degraded intracellularly, whereas C5aR releases ligand back extracellularly — supporting C5L2 as a recycling decoy receptor in humans. Engineered chimeric C5L2 with C5aR G-protein coupling sequences failed to restore Ca2+ signaling or beta-arrestin redistribution. Constitutive ligand-independent internalization assay, clathrin inhibition (dominant-negative), ligand retention/degradation tracking, Ca2+ assay, beta-arrestin redistribution assay in transfected cell lines Molecular immunology High 19100624
2009 C5L2 undergoes ligand-dependent (ASP and C5a) endocytosis that is clathrin- and cholesterol-dependent; following endocytosis, C5L2 traffics through early endosomes (Rab5), late endosomes (Rab7), and recycling endosomes (Rab11); the S323I mutation prevents C5L2 from localizing to the cell surface and abolishes ligand-mediated receptor phosphorylation and beta-arrestin-2 translocation, as well as downstream functional responses (glucose transport and TG synthesis). Beta-arrestin-2-GFP translocation, Rab-GFP co-localization by live imaging, receptor phosphorylation assay, functional glucose transport and TG synthesis assays in stably transfected C5L2-HEK cells; S323I mutant receptor Molecular immunology High 19615750
2009 C5a and C5a-desArg (but not C3a or C3a-desArg) stimulate beta-arrestin2 redistribution to cytoplasmic vesicles via C5L2; direct C5L2-beta-arrestin interaction confirmed by a beta-galactosidase fragment complementation assay; beta-arrestin coupling occurred at subnanomolar C5a concentrations. GFP-labeled beta-arrestin2 redistribution assay, beta-galactosidase fragment complementation assay in stably transfected cells Journal of biomolecular screening High 19641221
2010 C5L2-deficient mice are protected from OVA- and house dust mite-induced allergic asthma (reduced AHR, Th2 cytokines, eosinophilic inflammation, IgE, mucus); C5L2-deficient myeloid dendritic cells produce IL-23 and drive Th17 responses rather than Th2 responses upon HDM pulsing, indicating C5L2 on mDCs controls the Th1/Th17 versus Th2 balance. C5L2 KO mice, OVA and HDM asthma models, adoptive transfer of C5L2-deficient mDCs into WT mice, in vitro cytokine profiling of mDCs Journal of immunology High 20974988
2011 TLR activation induces C5a hypersensitivity by reducing C5L2 activity (not by upregulating C5aR); TLR-induced hypersensitivity was mimicked by C5L2 blockade and absent in C5L2 KO mice, confirming that TLRs amplify C5a responses by targeting C5L2 as a negative modulator of C5aR. PBMCs and whole blood with TLR ligand pretreatment, C5L2 KO mice, TLR4-deficient mice, C5L2 blocking antibody, C5a-induced cytokine readouts European journal of immunology High 21630250
2012 C5L2 and C5aR form constitutive homo- and heterodimers in HEK293 cells (by BRET); in adipocytes, ASP or C5a stimulation promotes internalization of C5L2 with increasing perinuclear co-localization with C5aR; C5L2 activation by ASP (but not C5a) increases fatty acid uptake/esterification in adipocytes, while both ligands activate Akt phosphorylation. BRET (bioluminescent resonance energy transfer) in HEK293 cells, confocal microscopy in 3T3-L1 adipocytes and J774 macrophages, fatty acid uptake assay, Western blotting Cellular signalling Medium 23268185
2013 C5L2 blockade with mAb in allergic contact dermatitis in mice dramatically increases inflammation, and this exacerbation is reversed by anti-C5aR mAb, demonstrating that C5L2 suppresses C5aR-mediated beta-arrestin signaling in vivo. C5L2 KO mice in murine contact sensitivity model, anti-C5aR mAb treatment, inflammatory readouts Journal of immunology High 24043888
2013 Ligation of both C5aR and C5L2 is required for optimal C5a-induced G-CSF production from peritoneal macrophages; C5a-mediated G-CSF induction is associated with PI3K/Akt and MEK1/2 signaling; G-CSF levels during CLP sepsis are reduced in both C5aR- and C5L2-deficient mice. C5aR KO and C5L2 KO mouse peritoneal macrophages, G-CSF ELISA, PI3K/MEK inhibitors, CLP sepsis model European journal of immunology High 23575697
2013 C5a, but not C5a-des Arg, induces upregulation of C5aR-C5L2 heteromer formation as measured by BRET; this heteromer formation is inhibited by a C5aR-specific antagonist; the two ligands produce differential IL-10 responses in macrophages, suggesting heteromerization contributes to differential signaling. BRET in transfected HEK293 cells, wide-field microscopy, ELISA in human monocyte-derived macrophages Immunology and cell biology Medium 24060963
2014 C5L2 physically interacts with C5aR and is required for optimal C5a-mediated C5aR internalization through an AP2-dependent, dynamin-dependent mechanism; without C5L2, AP2 recruitment to the receptor complex fails; C5L2-dependent C5aR internalization drives downstream MEK/ERK signaling. Co-immunoprecipitation, dynamin inhibitor (dynasore), AP2 recruitment assay, ERK phosphorylation in transfected cells; C5L2-deficient mice in acute colitis model Cellular signalling High 24631530
2015 In human mast cells (LAD2) expressing surface C5aR2 but not C5aR1, C5a induces ERK phosphorylation, cytokine production (GM-CSF, TNF, CXCL10, CCL2), adhesion, and chemotaxis via C5aR2; these responses depend on beta-arrestin-2 and PI3K; lentiviral shRNA silencing of C5aR2 renders cells unresponsive to all C5a-induced effects. Lentiviral shRNA knockdown of C5aR2, siRNA against beta-arrestin-2, wortmannin (PI3K inhibitor), ERK phosphorylation, ELISA, adhesion and chemotaxis assays in LAD2 cells Journal of immunology High 26283482
2016 C5L2-deficient mice (BALB/c) show more severe LPS-induced acute lung injury with greater airway edema, neutrophilia, MPO activity, and pro-inflammatory cytokines/chemokines; anti-C5aR blockade reverses neutrophilic infiltration in C5L2-/- mice, confirming C5L2's anti-inflammatory role is executed through negative modulation of C5aR. C5L2 KO mice, intranasal LPS model, anti-C5aR blocking antibody, BAL fluid analysis, lung homogenate cytokine measurement American journal of respiratory cell and molecular biology High 27285858
2016 Selective C5aR2 ligands (P32 and P59) selectively recruit beta-arrestin 2 via C5aR2, partially inhibit C5a-induced ERK1/2 activation, and reduce LPS-stimulated IL-6 release from macrophages without directly affecting C5aR1; P32 inhibits C5a-mediated neutrophil mobilization in WT but not C5aR2-/- mice. Peptide library screen, beta-arrestin 2 recruitment assay, ERK1/2 phosphorylation assay, IL-6 ELISA in human macrophages, in vivo neutrophil mobilization in C5aR2 KO mice Immunology and cell biology High 27108698
2017 C5aR2 expression is strongest in brain, bone marrow, and airways; all myeloid-derived cells express C5aR2 with neutrophils showing strong homogeneous expression; T cells are negative; B cells and NK cells express C5aR2. Selective C5aR2 ligation in neutrophils blocks C5a-driven ERK1/2 phosphorylation. Activation of C5aR2 in NK cells suppresses IL-12/IL-18-induced IFN-γ production. IL-33 challenge reduces C5aR2 in pulmonary eosinophils and monocyte-derived DCs. Floxed tdTomato-C5aR2 knock-in reporter mouse, flow cytometry, ERK1/2 phosphorylation assay in neutrophils, IFN-γ production assay in NK cells, intratracheal IL-33 challenge Journal of immunology High 28864475
2017 C5aR2-deficient mice show increased lesion volumes and worsened recovery from contusive spinal cord injury; acute PMX205 (C5aR1 antagonist) treatment improved outcomes in both WT and fully alleviated worsened recovery in C5aR2-/- mice, demonstrating C5aR2 is neuroprotective by restraining injurious C5aR1 signaling. C5aR2 KO mice, contusive SCI model, PMX205 C5aR1 antagonist treatment, lesion volume measurement, myelin sparing, behavioral recovery scores Journal of neurotrauma High 28173736
2018 C5ar2-/- mice show increased skin lesions in a bullous pemphigoid model while C5ar1-/- mice are protected, demonstrating opposing roles for C5aR1 (proinflammatory/pathogenic) and C5aR2 (anti-inflammatory/protective) in autoantibody-mediated tissue damage. C5ar1 KO and C5ar2 KO mice, anti-Col17 IgG transfer BP model, skin lesion scoring, neutrophil migration assay, PMX53 pharmacological C5aR1 inhibition Frontiers in immunology High 29599777
2018 CD10+GPR77+ (C5AR2+) cancer-associated fibroblasts sustain cancer stem cells through NF-κB activation driven by complement signaling via GPR77/C5AR2; GPR77 maintains persistent NF-κB p65 phosphorylation and acetylation; neutralizing anti-GPR77 antibody abolishes tumor formation and restores chemosensitivity. Patient-derived xenografts, anti-GPR77 neutralizing antibody, NF-κB reporter, p65 phosphorylation/acetylation assays, PDX co-injection experiments Cell High 29395328
2019 C5aR2 expressed on endothelial cells acts as an atypical chemoattractant receptor that transports C5a from the perivascular tissue into the vessel lumen (transcytosis); this transported C5a initiates C5aR1-mediated neutrophil arrest, while ACKR1-transported chemokines drive CXCR2-dependent neutrophil transmigration — establishing sequential roles of atypical receptors in neutrophil recruitment. Intravital microscopy in live mice, immune complex-induced arthritis model, C5aR2-deficient mice, ACKR1-deficient mice, in vivo tracking of C5a transport Science immunology High 31076525
2019 C5aR2 promotes NLRP3 inflammasome activation and HMGB1 release from macrophages by amplifying dsRNA-dependent PKR expression; PKR upregulation by C5a-C5aR2 interaction depends on MEK/ERK and type I IFN signaling pathways; C5aR2 deficiency restricts NLRP3 activation and HMGB1 release both in vitro and in vivo. C5aR2-deficient mice and macrophages, siRNA knockdown, immunoblotting, qRT-PCR for PKR expression, MEK inhibitor treatment, NLRP3 inhibition The Journal of biological chemistry High 30971430
2019 C5aR2 is required for C5a-mediated renal inflammation and tissue damage in acute pyelonephritis; C5aR2 signaling activates NLRP3/caspase-1 inflammasome and HMGB1 release in macrophages; blocking HMGB1 reduces C5aR2-mediated NLRP3 activation, placing HMGB1 upstream of NLRP3 in C5aR2 signaling. C5ar2 KO mice, uropathogenic E. coli bladder inoculation model, C5aR1-deficient macrophages (expressing only C5aR2), HMGB1 blocking antibody, NLRP3/caspase-1/IL-1β measurement JCI insight High 32191644
2020 Selective C5aR2 agonism (P32) by itself produces no detectable MAPK signaling but significantly dampens C5aR1-, C3aR-, and CMKLR1-mediated ERK signaling and alters intracellular calcium mobilization from these receptors; C5aR2 activation also reduces cytokine production from TLR2, TLR3, TLR4, TLR7, Dectin-1, Dectin-2, Mincle (reducing IL-6/TNF by 80-90%), and STING pathways in primary human macrophages. C5aR2 agonist P32 treatment of primary human monocyte-derived macrophages, ERK phosphorylation assay, Ca2+ mobilization, ELISA for multiple cytokines Journal of immunology High 32611725
2020 C5aR2 deficiency in intestinal IR injury worsens intestinal damage due to increased C5aR1-mediated neutrophil infiltration; C5aR1 blockade in C5aR2-/- mice prevents neutrophil accumulation and reduces pathology; C5aR2 deficiency also reduces circulating neutrophil numbers after IR via a C5aR1-independent mechanism, demonstrating distinct and separable functions of C5aR2. C5aR2 KO mice, intestinal IR model, PMX53 C5aR1 antagonist, neutrophil depletion, tissue damage scoring, cytokine measurement Journal of immunology High 33028618
2021 SB290157, widely used as a 'C3aR antagonist', is actually a partial agonist at C5aR2, mediating beta-arrestin recruitment at higher doses and significantly dampening C5a-induced ERK signaling in human and mouse primary macrophages via C5aR2. Beta-arrestin recruitment assay in transfected cells, ERK phosphorylation assay in primary macrophages, pharmacological profiling against C3aR, C5aR1, C5aR2 Frontiers in pharmacology Medium 33551801
2022 C5aR2 deficiency in neutrophils reduces intracellular calcium flux, ROS release, and migration capacity when activated with immune complexes or C5a; C5aR2 deficiency lowers the ratio of activating to inhibitory FcγRs on neutrophils; LysM-specific C5aR2 KO recapitulates global C5aR2 KO phenotype in epidermolysis bullosa acquisita. C5aR2 KO and LysM-Cre/C5aR2-flox mice, antibody transfer EBA model, in vitro Ca2+ flux, ROS assay, migration assay, FcγR expression analysis by flow cytometry The Journal of investigative dermatology High 35007559
2023 CRISPR-KO of C5aR2 in macrophages significantly increases STING-mediated IFN-β secretion; STING and IRF3 expression are increased in C5aR2 KO cells; transcriptomic analysis shows upregulation of nucleic acid sensing and antiviral signaling pathways in C5aR2 KO cells, indicating C5aR2 negatively regulates the cGAS-STING-IFN-β axis. CRISPR-Cas9 KO of C5aR2 in THP-1 cells and primary human monocyte-derived macrophages, ELISA for IFN-β, Western blot for STING/IRF3, RNA-seq Cells High 38067135
2025 C5aR2 on CD4+ T cells orchestrates Th1 cell contraction via a C5-C5aR2-prostacyclin (PGI2) axis: C5aR2 activation shifts prostaglandin balance from PGE2 to PGI2 production, which signals autocrine through PGI2 receptor to induce IL-1R2 expression; IL-1R2 sequesters Th1-driving intrinsic IL-1β, facilitating Th1 contraction. Disruption of this axis characterizes pathological Th1 persistence in CAPS, Crohn's disease, and RA. CD4+ T cell-intrinsic genetic and pharmacological dissection, prostaglandin profiling, IL-1R2 expression assay, T cell functional assays, human T cells from CAPS patients with PGE2 synthase inhibitor treatment Immunity High 40449486

Source papers

Stage 0 corpus · 99 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 CD10+GPR77+ Cancer-Associated Fibroblasts Promote Cancer Formation and Chemoresistance by Sustaining Cancer Stemness. Cell 997 29395328
2003 C5L2, a nonsignaling C5A binding protein. Biochemistry 211 12899627
2009 The C5a receptor (C5aR) C5L2 is a modulator of C5aR-mediated signal transduction. The Journal of biological chemistry 206 20044484
2001 The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg(74). The Journal of biological chemistry 189 11773063
2007 C5L2 is critical for the biological activities of the anaphylatoxins C5a and C3a. Nature 187 17322907
2013 Extracellular histones are essential effectors of C5aR- and C5L2-mediated tissue damage and inflammation in acute lung injury. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 181 23982144
2012 C5L2: a controversial receptor of complement anaphylatoxin, C5a. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 169 23239822
2005 An anti-inflammatory function for the complement anaphylatoxin C5a-binding protein, C5L2. The Journal of biological chemistry 167 16204243
2000 A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells. Molecular immunology 151 11090875
2003 The chemoattractant receptor-like protein C5L2 binds the C3a des-Arg77/acylation-stimulating protein. The Journal of biological chemistry 140 12540846
2005 C5L2 is a functional receptor for acylation-stimulating protein. The Journal of biological chemistry 138 15833747
2008 Receptors for complement C5a. The importance of C5aR and the enigmatic role of C5L2. Immunology and cell biology 121 18227853
2019 The Complement Receptor C5aR2: A Powerful Modulator of Innate and Adaptive Immunity. Journal of immunology (Baltimore, Md. : 1950) 114 31160390
2008 The human complement fragment receptor, C5L2, is a recycling decoy receptor. Molecular immunology 108 19100624
2005 Evidence for a functional role of the second C5a receptor C5L2. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 106 15784721
2010 A critical role for C5L2 in the pathogenesis of experimental allergic asthma. Journal of immunology (Baltimore, Md. : 1950) 79 20974988
2017 The Controversial C5a Receptor C5aR2: Its Role in Health and Disease. Journal of immunology research 65 28706957
2016 Discovery of functionally selective C5aR2 ligands: novel modulators of C5a signalling. Immunology and cell biology 63 27108698
2005 Changes in the novel orphan, C5a receptor (C5L2), during experimental sepsis and sepsis in humans. Journal of immunology (Baltimore, Md. : 1950) 63 15634936
2003 C5a mutants are potent antagonists of the C5a receptor (CD88) and of C5L2: position 69 is the locus that determines agonism or antagonism. The Journal of biological chemistry 62 14570896
2019 The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages. The Journal of biological chemistry 57 30971430
2007 Reduced adipose tissue triglyceride synthesis and increased muscle fatty acid oxidation in C5L2 knockout mice. The Journal of endocrinology 57 17641279
2011 TLR activation enhances C5a-induced pro-inflammatory responses by negatively modulating the second C5a receptor, C5L2. European journal of immunology 56 21630250
2006 Ligand specificity of the anaphylatoxin C5L2 receptor and its regulation on myeloid and epithelial cell lines. The Journal of biological chemistry 56 17068344
2005 Identification of complement 5a-like receptor (C5L2) from astrocytes: characterization of anti-inflammatory properties. Journal of neurochemistry 56 15715664
2018 Tissue Destruction in Bullous Pemphigoid Can Be Complement Independent and May Be Mitigated by C5aR2. Frontiers in immunology 49 29599777
2017 Monitoring C5aR2 Expression Using a Floxed tdTomato-C5aR2 Knock-In Mouse. Journal of immunology (Baltimore, Md. : 1950) 48 28864475
2006 The role of the N-terminal domain of the complement fragment receptor C5L2 in ligand binding. The Journal of biological chemistry 48 17158873
2020 C5aR2 Activation Broadly Modulates the Signaling and Function of Primary Human Macrophages. Journal of immunology (Baltimore, Md. : 1950) 47 32611725
2009 C5a-stimulated recruitment of beta-arrestin2 to the nonsignaling 7-transmembrane decoy receptor C5L2. Journal of biomolecular screening 43 19641221
2013 Functional roles for C5a and C5aR but not C5L2 in the pathogenesis of human and experimental cerebral malaria. Infection and immunity 42 24191300
2009 Recombinant C3adesArg/acylation stimulating protein (ASP) is highly bioactive: a critical evaluation of C5L2 binding and 3T3-L1 adipocyte activation. Molecular immunology 41 19767107
2020 The C5a/C5aR2 axis promotes renal inflammation and tissue damage. JCI insight 40 32191644
2013 Complement activation fragment C5a receptors, CD88 and C5L2, are associated with neurofibrillary pathology. Journal of neuroinflammation 39 23394121
2013 C5a, but not C5a-des Arg, induces upregulation of heteromer formation between complement C5a receptors C5aR and C5L2. Immunology and cell biology 39 24060963
2009 C5a- and ASP-mediated C5L2 activation, endocytosis and recycling are lost in S323I-C5L2 mutation. Molecular immunology 39 19615750
2007 Acylation-stimulating protein/C5L2-neutralizing antibodies alter triglyceride metabolism in vitro and in vivo. American journal of physiology. Endocrinology and metabolism 39 17711993
2019 Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation. Science immunology 38 31076525
2017 The Alternative Receptor for Complement Component 5a, C5aR2, Conveys Neuroprotection in Traumatic Spinal Cord Injury. Journal of neurotrauma 38 28173736
2017 Critical role for complement receptor C5aR2 in the pathogenesis of renal ischemia-reperfusion injury. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 37 28396344
2018 Enhanced activation of interleukin-10, heme oxygenase-1, and AKT in C5aR2-deficient mice is associated with protection from ischemia reperfusion injury-induced inflammation and fibrosis. Kidney international 36 29935951
2012 C5L2 and C5aR interaction in adipocytes and macrophages: insights into adipoimmunology. Cellular signalling 35 23268185
2015 The Novel Receptor C5aR2 Is Required for C5a-Mediated Human Mast Cell Adhesion, Migration, and Proinflammatory Mediator Production. Journal of immunology (Baltimore, Md. : 1950) 34 26283482
2012 C5L2 receptor disruption enhances the development of diet-induced insulin resistance in mice. Immunobiology 33 22622332
2019 C5a receptors C5aR1 and C5aR2 mediate opposing pathologies in a mouse model of melanoma. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 32 31298935
2013 Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis. Journal of immunology (Baltimore, Md. : 1950) 32 24043888
2013 The interaction between C5a and both C5aR and C5L2 receptors is required for production of G-CSF during acute inflammation. European journal of immunology 30 23575697
2013 A pro-inflammatory role of C5L2 in C5a-primed neutrophils for ANCA-induced activation. PloS one 29 23785491
2023 FAP, CD10, and GPR77-labeled CAFs cause neoadjuvant chemotherapy resistance by inducing EMT and CSC in gastric cancer. BMC cancer 28 37277751
2021 The "C3aR Antagonist" SB290157 is a Partial C5aR2 Agonist. Frontiers in pharmacology 28 33551801
2006 Identification of a novel C5L2 variant (S323I) in a French Canadian family with familial combined hyperlipemia. Arteriosclerosis, thrombosis, and vascular biology 28 16627811
2016 C5L2, the Second C5a Anaphylatoxin Receptor, Suppresses LPS-Induced Acute Lung Injury. American journal of respiratory cell and molecular biology 27 27285858
2014 High expression of C5L2 correlates with high proinflammatory cytokine expression in advanced human atherosclerotic plaques. The American journal of pathology 27 24819959
2017 Structure and characterization of a high affinity C5a monoclonal antibody that blocks binding to C5aR1 and C5aR2 receptors. mAbs 25 28952876
2012 Sphingosine kinase 1 mediation of expression of the anaphylatoxin receptor C5L2 dampens the inflammatory response to endotoxin. PloS one 25 22355325
2007 The ASP receptor C5L2 is regulated by metabolic hormones associated with insulin resistance. Biochemistry and cell biology = Biochimie et biologie cellulaire 25 17464341
2020 Absence of the C5a Receptor C5aR2 Worsens Ischemic Tissue Injury by Increasing C5aR1-Mediated Neutrophil Infiltration. Journal of immunology (Baltimore, Md. : 1950) 24 33028618
2019 Distinct roles of the anaphylatoxin receptors C3aR, C5aR1 and C5aR2 in experimental meningococcal infections. Virulence 24 31274379
2017 Complement C5a receptors C5L2 and C5aR in renal fibrosis. American journal of physiology. Renal physiology 24 28903945
2014 C5L2 is required for C5a-triggered receptor internalization and ERK signaling. Cellular signalling 24 24631530
2013 Deficiency of C5L2 increases macrophage infiltration and alters adipose tissue function in mice. PloS one 22 23630572
2013 C5aR and C5L2 act in concert to balance immunometabolism in adipose tissue. Molecular and cellular endocrinology 19 24397921
2015 Atheroprotective role of C5ar2 deficiency in apolipoprotein E-deficient mice. Thrombosis and haemostasis 17 26084965
2019 Differential effects of anaphylatoxin C5a on antigen presenting cells, roles for C5aR1 and C5aR2. Immunology letters 16 30959077
2019 C5L2 Regulates DMP1 Expression during Odontoblastic Differentiation. Journal of dental research 15 30702959
2011 Relationship between a novel polymorphism of the C5L2 gene and coronary artery disease. PloS one 15 21698200
2022 C5aR2 Deficiency Ameliorates Inflammation in Murine Epidermolysis Bullosa Acquisita by Regulating Fcγ Receptor Expression on Neutrophils. The Journal of investigative dermatology 13 35007559
2011 Relationship between type 2 diabetes mellitus and a novel polymorphism C698T in C5L2 in the Chinese Han population. Endocrine 12 22180093
2023 C5L2 modulates BDNF production in human dental pulp stem cells via p38α pathway. Scientific reports 11 36593314
2016 C5L2 Receptor Represses Brain-Derived Neurotrophic Factor Secretion in Lipoteichoic Acid-Stimulated Pulp Fibroblasts. Journal of dental research 11 28033061
2022 Differential expression of C5aR1 and C5aR2 in innate and adaptive immune cells located in early skin lesions of bullous pemphigoid patients. Frontiers in immunology 10 36466856
2019 The Second Receptor for C5a, C5aR2, Is Detrimental to Mice during Systemic Infection with Listeria monocytogenes. Journal of immunology (Baltimore, Md. : 1950) 10 31597707
2018 C5L2 Silencing in Human Pulp Fibroblasts Enhances Nerve Outgrowth Under Lipoteichoic Acid Stimulation. Journal of endodontics 10 30032862
2014 Association of immune and metabolic receptors C5aR and C5L2 with adiposity in women. Mediators of inflammation 10 24523571
2013 A novel polymorphism (901G > a) of C5L2 gene is associated with coronary artery disease in Chinese Han and Uyghur population. Lipids in health and disease 10 24073849
2022 C5aR2 receptor: The genomic twin of the flamboyant C5aR1. Journal of cellular biochemistry 9 35977039
2013 Circulating C5L2 gene polymorphism is associated with type 2 diabetes mellitus in Saudi population. Molecular biology reports 9 24078164
2021 Role of C5aR1 and C5L2 Receptors in Ischemia-Reperfusion Injury. Journal of clinical medicine 8 33801177
2017 Association of C5L2 genetic polymorphisms with coronary artery disease in a Han population in Xinjiang, China. Oncotarget 8 28052000
2024 C5L2 CRISPR KO enhances dental pulp stem cell-mediated dentinogenesis via TrkB under TNFα-induced inflammation. Frontiers in cell and developmental biology 7 38318114
2023 The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita. Frontiers in immunology 7 37275893
2022 Neutraligands of C5a can potentially occlude the interaction of C5a with the complement receptors C5aR1 and C5aR2. Journal of cellular biochemistry 7 36565188
2014 Complement receptors C5aR and C5L2 are associated with metabolic profile, sex hormones, and liver enzymes in obese women pre- and postbariatric surgery. Journal of obesity 7 24796007
2019 Selective and marked decrease of complement receptor C5aR2 in human thoracic aortic aneurysms: a dysregulation with potential inflammatory effects. Open heart 6 31798913
2017 Corrigendum to "The Controversial C5a Receptor C5aR2: Its Role in Health and Disease". Journal of immunology research 6 29226158
2013 Relationship of C5L2 receptor to skeletal muscle substrate utilization. PloS one 6 23460866
2023 Ternary model structural complex of C5a, C5aR2, and β-arrestin1. Journal of biomolecular structure & dynamics 5 37493401
2025 A CD4+ T cell-intrinsic complement C5aR2-prostacyclin-IL-1R2 axis orchestrates Th1 cell contraction. Immunity 4 40449486
2024 Role of the Anaphylatoxin Receptor C5aR2 in Angiotensin II-Induced Hypertension and Hypertensive End-Organ Damage. American journal of hypertension 4 38934290
2014 A novel mutation in C5L2 gene was associated with hyperlipidemia and retinitis pigmentosa in a Chinese family. Lipids in health and disease 4 24885523
2024 Emerging role of C5aR2: novel insights into the regulation of uterine immune cells during pregnancy. Frontiers in immunology 3 38979410
2023 C5aR2 Regulates STING-Mediated Interferon Beta Production in Human Macrophages. Cells 3 38067135
2008 [Role of progesterone in acylation stimulating protein-receptor C5L2 pathway in adipocytes and preadipocytes]. Zhonghua yi xue za zhi 3 18353218
2025 C5L2 gene polymorphisms and their functional interaction with metabolic-inflammatory networks in T2DM-associated CHD: insights from an integrative genetic and clinical analysis in a Chinese population. Frontiers in cardiovascular medicine 2 41103368
2011 S323I polymorphism of the C5L2 gene was not identified in a Chinese population with familial combined hyperlipidemia or with type 2 diabetes. Genetics and molecular research : GMR 2 22194190
2007 [Expression of acylation stimulating protein receptor (C5L2) in preadipocytes during differentiation and under stimulation of free fatty acids]. Zhonghua yi xue za zhi 2 18067837
2020 Correction: Selective and marked decrease of complement receptor C5aR2 in human thoracic aortic aneurysms: a dysregulation with potential inflammatory effects. Open heart 1 32509317
2024 C5aR2 Deficiency Lessens C5aR1 Distribution and Expression in Neutrophils and Macrophages. Journal of immunology research 0 39021433
2024 C5aR2 in Breast Cancer and Its Relationship with Clinicopathological Features. Journal of the College of Physicians and Surgeons--Pakistan : JCPSP 0 39648378