Affinage

FCGR2A

Low affinity immunoglobulin gamma Fc region receptor II-a · UniProt P12318

Length
317 aa
Mass
35.0 kDa
Annotated
2026-06-09
100 papers in source corpus 48 papers cited in narrative 48 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FCGR2A (FcγRIIa/CD32A) is a low-affinity activating IgG Fc receptor that couples antibody/immune-complex recognition to phagocytosis, oxidative burst, mediator release, and platelet activation across myeloid, dendritic, mast cell, and platelet lineages (PMID:1532752, PMID:8464427, PMID:16785568). Ligand recognition occurs through the lower hinge and adjacent CH2 region of IgG Fc, distinct from the CH2–CH3 surface used by protein A and FcRn, and extends to IgG3, IgG4, and the acute-phase pentraxin CRP in an allele-dependent manner (R131 versus H131) (PMID:10799893, PMID:10397151, PMID:10675363, PMID:15878871). Unlike other Fcγ receptors, FcγRIIa carries its signaling apparatus in its own cytoplasmic tail, an ITAM whose tyrosines are required and sufficient for phagocytosis without accessory FcRγ chain (PMID:7718892, PMID:7521687, PMID:1532752). Engagement drives Src-family kinase phosphorylation of the receptor within cholesterol-rich, flotillin-positive lipid rafts, followed by Syk recruitment, PLCγ and PI3K activation, IP3 generation, and Ca2+ flux (PMID:8144900, PMID:11441091, PMID:12508114, PMID:15130090); raft association also gates efficient IgG binding, and the receptor functions as a noncovalent surface dimer in which the dimer interface controls signaling rather than ligand binding (PMID:19494328, PMID:16751395). A cytoplasmic L-T-L motif routes calcium waves to the phagosome to enable phagolysosome fusion, and internalized receptor–ligand complexes are sorted to lysosomes for degradation (PMID:12676989, PMID:20736173). Signaling is restrained by SHP-1, which docks on the N-terminal ITAM tyrosine, and by co-ligated inhibitory partners PECAM-1 and CD300a; monovalent engagement can convert the ITAM to an inhibitory (ITAMi) mode that recruits SYK and SHP-1 to suppress VAV-1 and IRAK-1 (PMID:12832410, PMID:12893767, PMID:17588661, PMID:25061875). In platelets, FcγRIIa drives IgG-immune-complex- and integrin-coupled activation requiring BTK, 12-lipoxygenase, and the β3 integrin cytoplasmic domain, and this axis underlies antibody-mediated thrombocytopenia, drug-dependent and tumor-cell-induced platelet activation, anaphylaxis, and lupus-associated thrombosis (PMID:25100742, PMID:31809536, PMID:19197137, PMID:10201963, PMID:24258815, PMID:29654057, PMID:33331924). FcRn serves as an acidic-condition coreceptor forming a ternary complex with CD32a to license immune-complex-driven inflammatory responses (PMID:32658257).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1992 High

    Established that FcγRIIa's own cytoplasmic domain is required and sufficient for phagocytosis, distinguishing it from receptors that require accessory subunits.

    Evidence Reconstitution of FcγRIIa, tail-minus, and FcγRIIb1 constructs in 3T6 fibroblasts with cytochalasin D controls

    PMID:1532752

    Open questions at the time
    • Did not define the signaling motif within the tail
    • Fibroblast model lacks native myeloid effectors
  2. 1995 High

    Identified the cytoplasmic ITAM as the activating module, mapping individual tyrosines required for phagocytosis and contrasting it with the inhibitory ITIM of FcγRIIb.

    Evidence Site-directed mutagenesis of cytoplasmic tyrosines in COS-1 and B cells with phagocytosis, phosphorylation, and Ca2+ readouts

    PMID:7521687 PMID:7718892

    Open questions at the time
    • Did not identify the kinases acting on the ITAM
    • Relied on heterologous cell systems
  3. 2001 High

    Defined the proximal kinase cascade, showing Src-family kinases phosphorylate the receptor and recruit Syk and PI3K acting in parallel.

    Evidence Fcγ-p85 chimera, kinase-inactive Syk mutants, Syk inhibitors, and Src-deficient cells with PLCγ/Shc/Ca2+ readouts in macrophages and fibroblasts

    PMID:11441091 PMID:7612894 PMID:8144900 PMID:8405229

    Open questions at the time
    • Redundancy among Src-family kinases not fully resolved
    • Ordering of PI3K versus Syk branches partly inferred pharmacologically
  4. 2000 High

    Mapped the IgG binding site to the lower hinge/CH2 region, distinguishing FcγRIIa engagement from FcRn and protein A and explaining non-competition.

    Evidence IgG lower-hinge mutagenesis (LL234,235AA) and competition binding with recombinant soluble FcγRIIa, FcRn, and protein A

    PMID:10397151 PMID:10799893

    Open questions at the time
    • Did not address dynamic affinity regulation on cells
    • IgG4 binding shown biochemically without cellular confirmation
  5. 2003 High

    Showed lipid raft localization and noncovalent dimerization govern receptor phosphorylation and downstream actin remodeling, separating signaling control from ligand binding.

    Evidence Raft disruption agents, Src inhibitors, Y298F mutagenesis, flotillin-DRM fractionation, protein complementation, and dimer-interface mutagenesis in neutrophils and BHK cells

    PMID:11937562 PMID:12508114 PMID:15130090 PMID:16751395 PMID:19494328

    Open questions at the time
    • Structural basis of dimer-driven signaling enhancement unresolved
    • Physiological trigger for raft recruitment versus phosphorylation ordering still debated within the data
  6. 2003 High

    Identified negative-feedback regulators, establishing SHP-1 docking on the N-terminal ITAM tyrosine and PECAM-1/CD300a co-ligation as brakes on activation.

    Evidence Phosphopeptide mapping, ITAM tyrosine mutants, co-IP, NF-κB reporters in THP-1; FRET and reciprocal co-IP in platelets; co-ligation ROS assays in neutrophils

    PMID:12832410 PMID:12893767 PMID:17588661

    Open questions at the time
    • Quantitative balance of activating versus inhibitory inputs in vivo unclear
    • CD300a/PECAM-1 partner findings are Medium-confidence single-lab
  7. 2003 High

    Linked receptor signaling geometry to organelle function, showing the cytoplasmic L-T-L motif routes calcium waves to the phagosome for phagolysosome fusion.

    Evidence L-T-L motif mutagenesis with high-speed calcium wave imaging and phagolysosome fusion assays with Rab5/Rab7/LAMP-1 markers

    PMID:12676989

    Open questions at the time
    • Effectors decoding the calcium spatial signal not identified
    • Single-lab finding
  8. 2002 High

    Extended ligand recognition beyond IgG by showing CRP signals through the FcγRIIa ITAM in an allele-specific manner, defining R131 as the high-avidity CRP receptor.

    Evidence Allele-specific blocking mAb, genotyped donor binding/Ca2+ assays, CRP mutagenesis, and HL-60 phosphorylation of FcγRIIa/Syk/PLCγ2

    PMID:10675363 PMID:11801683 PMID:15878871

    Open questions at the time
    • In vivo significance of CRP–FcγRIIa signaling not established here
    • Monomeric versus aggregated CRP signaling equivalence is Medium-confidence
  9. 2010 High

    Defined the trafficking fate distinguishing FcγRIIa from FcγRIIb2, showing FcγRIIa delivers ligand to lysosomes for degradation via multimerization.

    Evidence Comparative fluorescent ligand tracking in ts20 fibroblasts with Src inhibitors and ubiquitylation-deficient mutants

    PMID:20736173

    Open questions at the time
    • Sorting machinery mediating lysosomal routing not identified
    • Heterologous fibroblast model
  10. 2014 High

    Established platelet-specific effectors and the inhibitory ITAMi mode, identifying 12-LOX as an essential downstream node and a single tyrosine (Y304) governing SYK/SHP-1-mediated suppression.

    Evidence 12-LOX inhibition and KO transgenic mice; Y304 mutagenesis, SYK/SHP-1 co-IP, arthritis model, and RA patient cells

    PMID:25061875 PMID:25100742

    Open questions at the time
    • Switch between activating and ITAMi modes in disease incompletely defined
    • 12-LOX mechanistic step within the cascade not fully placed
  11. 2019 High

    Identified BTK and TULA-2/miR-148a as additional regulators of FcγRIIa platelet and neutrophil signaling, providing pharmacological entry points.

    Evidence Multiple BTK inhibitors with HIT serum and human dosing; FLIM receptor proximity with TLR4; miR-148a inhibition and TULA-2 knockdown in transgenic mice

    PMID:23239500 PMID:26516227 PMID:31809536

    Open questions at the time
    • Direct enzymatic relationship of BTK to the receptor not biochemically resolved
    • TLR4 crosstalk finding is Medium-confidence single-lab
  12. 2020 High

    Demonstrated FcRn acts as a CD32a coreceptor forming an acidic-condition ternary complex required for immune-complex-driven immune responses, with the H131 variant binding more avidly.

    Evidence Co-IP/ternary complex assays, FcRn-deficient cells, allele comparison, and FcRn blockade in an RA mouse model

    PMID:32658257

    Open questions at the time
    • Structural basis of the ternary complex not defined
    • Generality across cell types beyond those tested unresolved
  13. 2022 High

    Mapped the FcγRIIa axis onto disease pathophysiology, implicating it in thrombocytopenia, anaphylaxis, lupus nephritis/thrombosis, glomerular neutrophil capture, tumor-cell-induced platelet secretion, and COVID-19 platelet hyperactivation, and validated therapeutic blockade.

    Evidence Transgenic and FcRγ-KO mouse models, catch-bond biophysics and intravital microscopy, patient sera/plasma, and anti-FcγRIIa antibody (VIB9600) across multiple disease models

    PMID:10201963 PMID:12960360 PMID:17046568 PMID:19197137 PMID:24258815 PMID:25470559 PMID:28891817 PMID:29654057 PMID:30459279 PMID:30610165 PMID:30692520 PMID:33331924 PMID:35309299 PMID:8027554

    Open questions at the time
    • Relative contribution of FcγRIIa versus other receptors in individual human diseases not fully quantified
    • Some disease-context findings are Medium-confidence single-lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the activating-versus-ITAMi decision, raft recruitment, dimerization, and coreceptor (FcRn) engagement are integrated into a single quantitative threshold for cell activation in vivo remains unresolved.
  • No unified structural model linking dimerization, raft entry, and ITAM phosphorylation thresholds
  • Mechanism converting monovalent engagement to inhibitory signaling in human disease incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0001618 virus receptor activity 4 GO:0060089 molecular transducer activity 4 GO:0038024 cargo receptor activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005764 lysosome 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-109582 Hemostasis 4 R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3 R-HSA-5653656 Vesicle-mediated transport 3
Partners
CD300AFCRNGRB2MAC-1PECAM-1PLCG2SHP-1SYK

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 The cytoplasmic domain of FcγRIIa contains an immunoreceptor tyrosine-based activation motif (ITAM) that is critical for B-cell activation and phagocytosis of opsonized bacteria. Mutation of the ITAM tyrosines in FcγRIIa abolished these activating functions, while the ITIM in FcγRIIb isoforms mediated inhibitory functions including downregulation of [Ca2+]i. B-cell transfection with wild-type or ITAM/ITIM tyrosine mutant FcγRII constructs; phagocytosis assays; tyrosine phosphorylation assays Blood High 7718892
1994 FcγRIIa mediates phagocytosis through its cytoplasmic ITAM tyrosines (Y275/Y1, Y282/Y2, Y298/Y3). Disruption of either Y-x-x-L motif (Y2 or Y3) inhibited phagocytosis 50–65% and reduced receptor tyrosine phosphorylation; replacement of Y1 alone had no effect, but Y1 substitution in mutants lacking Y2 or Y3 virtually eliminated both phagocytosis and phosphorylation. Site-directed mutagenesis of cytoplasmic tyrosines; COS-1 cell transfection; phagocytosis assays; tyrosine phosphorylation assays Blood High 7521687
1994 Cross-linking of FcγRIIa in macrophages leads to tyrosine phosphorylation of Shc, PLC-γ1, and p72Syk, generation of IP3, and [Ca2+]i flux. Phosphorylated FcγRIIa co-precipitates with activated PLC-γ1. Mutant receptors that fail to trigger [Ca2+]i flux also fail to phosphorylate Shc or PLC-γ1. Transfection of mouse macrophage cell line with human FcγRIIa; co-immunoprecipitation; tyrosine phosphorylation assays; IP3 measurement; Ca2+ flux Journal of immunology High 8144900
1992 FcγRIIa, but not the tail-minus variant or FcγRIIb1, mediates phagocytosis of IgG-opsonized erythrocytes when expressed in mouse fibroblasts, demonstrating that the cytoplasmic domain of FcγRIIa is required and sufficient for phagocytosis in the absence of other Fc receptor subunits. Stable transfection of 3T6 fibroblasts with FcγRIIa, tail-minus FcγRII, or FcγRIIb1 cDNA; phagocytosis assays; cytochalasin D blockade Blood High 1532752
2001 FcγRIIa signal transduction leading to phagocytosis proceeds via sequential activation of Src-family kinases → Syk and PI3K (acting in parallel). FcγRIIa is phosphorylated by an Src family member, which recruits and activates Syk and PI3K; Syk acts in parallel with PI3K downstream of Src. FcγRI-p85 chimera co-transfection; kinase-inactive Syk mutants; pharmacological Syk inhibitor; phagocytosis assays Journal of immunology High 11441091
1993 FcγRIIa can be phosphorylated on tyrosine and mediate phagocytosis in fibroblasts deficient in Src kinase, indicating Src is not strictly required. The Src-related kinase Fyn can also phosphorylate FcγRIIa in vitro, suggesting functional redundancy among Src-family kinases for receptor phosphorylation. Src-deficient fibroblast transfection; phagocytosis assays; in vitro kinase assays with Src and Fyn Experimental hematology Medium 8405229
1995 Cross-linking of FcγRIIa on neutrophils activates Src-family tyrosine kinases and Syk, leading to phosphorylation of Shc and PLC-γ isoforms, IP3 generation, and [Ca2+]i transient. GPI-anchored FcγRIIIb appears to synergize with FcγRIIa by utilizing the FcγRIIa signaling apparatus. Cross-linking experiments in neutrophils; tyrosine phosphorylation; Ca2+ flux; pharmacological inhibitors Seminars in immunology Medium 7612894
2000 FcγRIIa binds to the lower hinge and adjacent CH2 domain of IgG Fc, not the CH2-CH3 interface. Mutations LL234,235AA in the lower hinge abrogated binding of recombinant soluble FcγRIIa to human IgG1. FcγRIIa did not compete with protein A or FcRn (which bind CH2-CH3 interface) for IgG binding. Competition binding assays with recombinant soluble FcγRIIa, protein A and FcRn; IgG lower-hinge mutagenesis; SPR/binding assays Journal of immunology High 10799893
2003 FcγRIIa on plasmacytoid dendritic cells (NIPC/PDC) is required for IFN-α production induced by apoptotic cells combined with lupus IgG immune complexes. Blocking the FcγRIIa,c (CD32) ligand-binding site with specific antibody abrogated this IFN-α induction; Fab/F(ab')2 of SLE-IgG were ineffective, confirming Fc-dependence. RT-PCR on purified PDC confirmed FcγRIIa (not IIb or IIc) expression. Blocking anti-FcγR antibodies; Fab/F(ab')2 fragments of SLE-IgG; flow cytometry; RT-PCR on sorted PDC; PBMC IFN-α production assays Journal of immunology High 12960360
1994 ANCA IgG (but not IgM) binds ANCA target antigens expressed on neutrophil surfaces and engages the FcγRIIa ligand-binding site, triggering an oxidative burst. Blockade of FcγRIIa with a binding-site-specific Fab significantly reduced ANCA IgG-triggered reactive oxygen species production. The FcγRIIa allelic phenotype (R131 vs H131) influenced the magnitude of ROS production by more than threefold. Neutrophil oxidative burst assays (dihydrorhodamine oxidation); FcγRIIa blocking Fab; ANCA IgG vs IgM comparison; allele-stratified donor studies Journal of immunology High 8027554
2000 CRP binds with high affinity to FcγRIIa on monocytes and neutrophils in an allele-specific manner: CRP binds with high avidity to FcγRIIA R-131 homozygotes and initiates [Ca2+]i increases; binding is reduced in H-131 homozygotes. This demonstrates a reciprocal relationship between IgG2 and CRP binding avidities for FcγRIIa alleles, with R131 being the high-affinity CRP receptor. Flow cytometry binding assays with CRP on monocytes/neutrophils from genotyped donors; allele-specific blocking mAb (41H16); [Ca2+]i measurements; IFN-γ enhancement studies Journal of clinical investigation High 10675363
2005 Site-directed mutagenesis of CRP identified residues Thr173 and Asn186 as critical for CRP binding to FcγRIIa. Lys114 and Leu176 are important for binding to FcγRI but not FcγRIIa. These binding sites partially overlap with the C1q-binding site on CRP. Site-directed mutagenesis of CRP; baculovirus expression of recombinant CRP mutants; FcγRIIa and FcγRI binding assays Journal of biological chemistry High 15878871
2002 CRP at acute-phase concentrations signals through FcγRIIa in granulocytic HL-60 cells, inducing phosphorylation of FcγRIIa itself, Syk kinase, and PLCγ2, with translocation of PLCγ2 and PI3K to the membrane. Both aggregated and monomeric cross-linked CRP generate signals of similar intensity through the FcγRIIa ITAM. Phosphorylation assays in HL-60 granulocytes; membrane fractionation; comparison of aggregated vs. monomeric CRP Journal of immunology Medium 11801683
2003 SHP-1 phosphatase associates specifically with the phosphorylated N-terminal ITAM tyrosine of FcγRIIa following receptor clustering, while Syk associates with the C-terminal ITAM tyrosine. SHP-1 association suppresses total cellular tyrosine phosphorylation and downregulates NF-κB-dependent gene transcription. SHP-1 also forms complexes with Syk, p85-PI3K, and p62dok upon FcγRIIa clustering. Synthetic phosphopeptides; stable transfection of ITAM tyrosine mutants of FcγRIIa in THP-1 cells; co-immunoprecipitation; NF-κB reporter assays; SHP-1 overexpression Journal of biological chemistry High 12832410
2003 FcγRIIa phosphorylation by Src-family kinases residing in lipid rafts (DRMs) is required for receptor-induced actin rearrangement and capping. After cross-linking, FcγRIIa is recruited to DRMs where it co-localizes with Lyn kinase. Disruption of DRMs or Lyn membrane anchoring blocked FcγRIIa phosphorylation and capping. Mutation of Y298 (ITAM tyrosine) in FcγRIIa abolished phosphorylation, capping, and receptor-mediated cell spreading. DRM disruption (beta-cyclodextrin, hydroxymyristic acid, bromopalmitate); Src kinase inhibitors (PP1, herbimycin A); Y298F BHK cell transfection; sucrose gradient fractionation; confocal microscopy Journal of cell science High 12508114
2002 Cross-linking of FcγRIIa in human neutrophils leads to its rapid translocation into detergent-insoluble (non-raft) fractions within seconds, followed by degradation within minutes. This degradation requires Src kinase activity and cholesterol-containing membrane microdomains, but not PI3K or other tested kinases. FcγRIIa cross-linking; Triton X-100 insolubility assays; sucrose gradient fractionation; Src inhibitor PP1; wortmannin; filipin cholesterol depletion; flow cytometry Journal of immunology Medium 11937562
2004 Cross-linking of FcγRIIa (CD32A) in neutrophil plasma membranes recruits it to high-density flotillin-1-positive detergent-resistant membranes (DRMs), a process that precedes and is independent of tyrosine phosphorylation. Tyrosine phosphorylation of FcγRIIa and Syk in these membranes requires Src kinase activity. Neutrophil plasma membrane preparation; FcγRIIa cross-linking; sucrose gradient DRM isolation; Src inhibitor PP2; methyl-β-cyclodextrin treatment; tyrosine phosphorylation assays Biochemical journal Medium 15130090
2003 The L-T-L motif in the cytoplasmic domain of FcγRIIa controls the spatiotemporal routing of calcium waves to the phagosome. Mutation of the L-T-L motif prevents proper calcium signal routing to the phagosome (but not around the plasma membrane), and FcγRIIa-L-T-L mutants fail to support phagolysosome fusion despite normal recruitment of LAMP-1, Rab5, and Rab7. L-T-L motif mutagenesis; high-speed calcium microscopy (wave mapping); phagolysosome fusion assays; LAMP-1/Rab5/Rab7 localization Proceedings of the National Academy of Sciences High 12676989
2006 FcγRIIa exists as a noncovalent dimer on the cell surface. Protein complementation studies confirmed close molecular association of FcγRIIa molecules. Mutagenesis of the crystallographically-identified dimer interface did not affect IgG ligand binding but significantly altered the magnitude and kinetics of receptor phosphorylation, indicating that dimerization is required for normal FcγRIIa signaling. Protein complementation assays; site-directed mutagenesis of dimer interface; ligand binding assays; receptor phosphorylation kinetics; crystallographic analysis of dimer interface Journal of immunology High 16751395
1999 Recombinant FcγRIIa binds IgG3 (KD = 0.6 μM) and also IgG4 (KD = 3 μM), establishing FcγRIIa as an IgG4 receptor. Both potential N-linked glycosylation sites are occupied. Crystal quality diffracting to 2.1 Å were obtained, establishing the first crystallisation of FcγRIIa. Equilibrium binding analysis; baculovirus-expressed recombinant FcγRIIa; ESMS glycan analysis; X-ray crystallography Immunology letters Medium 10397151
2009 Association of FcγRIIa with lipid rafts is required for efficient IgG ligand binding. Cholesterol depletion/sequestration greatly reduced FcγRIIa-mediated IgG binding. FcγRIIa mutants with reduced lipid raft association (A224S, C241A) showed decreased IgG binding; constitutively raft-associated GPI-anchored FcγRIIa showed increased IgG binding. Lipid raft disruption (methyl-β-cyclodextrin, filipin); site-directed mutagenesis (A224S, C241A); GPI-anchored FcγRIIa expression; flow cytometry IgG binding assays Journal of immunology High 19494328
2010 FcγRIIa and FcγRIIB2 sort to distinct intracellular compartments after IgG immune complex internalization: FcγRIIa is delivered with its ligand to lysosomes for degradation, while FcγRIIB2 dissociates from ligand and recycles. FcγRIIa lysosomal sorting requires receptor multimerization but not Src kinase activity or receptor lysine ubiquitylation. FcγRIIa and FcγRIIB2 expression in ts20 fibroblasts; fluorescent ligand tracking; lysosomal vs. recycling compartment markers; Src inhibitors; ubiquitylation-deficient lysine mutants Journal of biological chemistry High 20736173
1999 FcγRIIa transgenic mice (expressing human FcγRIIa on platelets and macrophages at human physiologic levels) show significantly more severe antibody-mediated thrombocytopenia than wild-type mice. In FcγRIIa transgenic × FcRγ-chain knockout mice, severe immune thrombocytopenia still occurs, demonstrating that FcγRIIa mediates platelet clearance independently of FcRγ-chain (i.e., independently of FcγRI and FcγRIII). FcγRIIa transgenic mouse generation; FcRγ-chain knockout crosses; in vivo anti-platelet antibody-induced thrombocytopenia model; platelet counting Journal of immunology High 10201963
2000 In resting neutrophils, FcγRIIa (CD32A) is in a low-affinity state and cells preferentially use FcγRIIIB for immune complex binding. Activation with fMLP converts FcγRIIa to a high-affinity state, increasing CD32A-dependent rosetting ~5-fold without increasing CD32A surface expression. This affinity upregulation is cell-type-specific and not observed in CHO cells expressing CD32A. CD16B-deficient donor neutrophils; anti-CD16 blocking; fMLP activation; EA rosetting assays; immune complex binding; CHO cell transfection comparison Blood High 10648424
2006 Platelet FcγRIIa binds and internalizes IgG-containing immune complexes. Wild-type mouse platelets (lacking Fcγ receptors) did not bind or endocytose IgG complexes, while transgenic FcγRIIa-expressing mouse platelets bound and internalized them, as confirmed by flow cytometry and electron microscopy. FcγRIIa transgenic mouse platelets; flow cytometry; electron microscopy; IgG complex internalization assays Experimental hematology High 17046568
2014 Inhibitory engagement of the FcγRIIa ITAM (ITAMi signaling) via anti-FcγRII F(ab')2 or IVIg ameliorates arthritis. ITAMi signaling through FcγRIIa requires a single tyrosine (Y304) and leads to recruitment of SYK and SHP-1, inhibition of VAV-1 (reducing ROS) and IRAK-1 (reducing IL-1-driven cytokines). This converts activating ITAM signaling to an inhibitory mode. FcγRIIa transgenic mouse arthritis model; anti-FcγRII F(ab')2 treatment; Y304 mutagenesis; SYK and SHP-1 co-immunoprecipitation; ROS and cytokine assays; RA patient synovial cell experiments Journal of clinical investigation High 25061875
2014 Platelet 12(S)-lipoxygenase (12-LOX) is an essential component downstream of FcγRIIa signaling. Pharmacological inhibition of 12-LOX significantly attenuated FcγRIIa-mediated platelet aggregation, and abrogated FcγRIIa-induced PLCγ2 activity, Ca2+ mobilization, Rap1 activation, PKC activation, and αIIbβ3 integrin activation. FcγRIIa transgenic mice deficient in platelet 12-LOX failed to form normal aggregates. 12-LOX pharmacological inhibition in human platelets; FcγRIIa transgenic × 12-LOX-deficient mouse model; PLCγ2, Ca2+, Rap1, PKC, αIIbβ3 activation assays Blood High 25100742
2003 PECAM-1 (CD31) is physically proximal to FcγRIIa on the platelet membrane and functionally downregulates FcγRIIa-mediated signaling. Co-ligation of PECAM-1 with FcγRIIa inhibited PLCγ2 activation, Ca2+ mobilization, and PI3K-dependent signaling. Physical proximity was confirmed by FRET and co-immunoprecipitation. Co-immunoprecipitation; FRET; anti-PECAM-1 and anti-FcγRIIa Fab blocking; platelet aggregation assays; PLCγ2, Ca2+, PI3K activation assays Blood High 12893767
2009 Eptifibatide-dependent patient antibodies activate platelets through FcγRIIa: patient IgG plus eptifibatide induced platelet secretion, aggregation, and tyrosine phosphorylation of FcγRIIa, Syk, and PLCγ2. Fab fragments of anti-FcγRIIa mAb IV.3 blocked all activation. Platelets lacking the integrin β3 cytoplasmic domain were not activated despite normal FcγRIIa expression, revealing a required FcγRIIa–β3 cytoplasmic domain cooperativity. Human platelet activation assays; anti-FcγRIIa IV.3 Fab blockade; Glanzmann thrombasthenia β3-truncation patient platelets; phosphorylation assays; aggregation/secretion assays Journal of clinical investigation High 19197137
2013 FcγRIIa plays an essential and central role in tumor cell-induced platelet secretion (TCIPS). Pharmacological antagonists of Syk, PLCγ, and PKC (all downstream ITAM effectors) were the most potent inhibitors of TCIPS. FcγRIIa was demonstrated to mediate platelet–tumor cell cross-talk leading to dense granule secretion that precedes and is required for aggregation. Pharmacological ITAM pathway inhibitors; platelet-tumor cell co-incubation (Caco-2, PC3M-luc, MDA-MB-231, MCF-7); dense granule secretion assays; aggregation assays Blood Medium 24258815
2017 Neutrophil FcγRIIa promotes glomerular neutrophil capture via Abl/Src tyrosine kinase-mediated F-actin polymerization. FcγRIIa-IgG bonds increase in lifetime ('catch bond') under mechanical force in an F-actin-dependent manner. Inhibiting Abl/Src with bosutinib reduced FcγRIIa-mediated glomerular neutrophil accumulation and renal injury in crescentic anti-GBM nephritis. In vitro neutrophil capture under flow; biophysical FcγRIIa-IgG bond lifetime measurements; kidney intravital microscopy; Abl/Src inhibitor bosutinib; anti-GBM nephritis mouse model Journal of clinical investigation High 28891817
2015 miR-148a-3p targets and inhibits TULA-2 mRNA, which is a negative regulator of FcγRIIa-mediated platelet activation. In vivo inhibition of miR-148a in FcγRIIa transgenic mice upregulated TULA-2, reduced FcγRIIa-mediated αIIbβ3 activation and Ca2+ mobilization, and decreased thrombus formation after intravascular FcγRIIa activation. Genome-wide platelet expression profiling; siRNA knockdown of TULA-2 in HEL cells; anti-miR-148a administration in FcγRIIa transgenic mice; platelet activation and thrombus formation assays Blood High 26516227
2019 BTK (Bruton's tyrosine kinase) acts downstream of FcγRIIa in platelet activation. All tested BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib, tirabrutinib, evobrutinib, fenebrutinib) blocked FcγRIIa-mediated platelet aggregation, secretion, P-selectin expression, and platelet-neutrophil complex formation. Ibrutinib oral administration in a single dose was sufficient to suppress platelet FcγRIIa activation. BTK inhibitor pharmacological studies in human whole blood; anti-FcγRIIa cross-linking; HIT patient serum activation assay; oral ibrutinib dosing in human volunteers Blood advances High 31809536
2012 Bruton's tyrosine kinase (BTK) mediates FcγRIIa/TLR-4 receptor crosstalk in human neutrophils. LPS exposure shortens the molecular distance between FcγRIIa and TLR4 on neutrophils. Stimulation of LPS-primed neutrophils with anti-IL-8:IL-8 immune complexes activates TLR4 cascade via FcγRIIa engagement through a BTK-dependent mechanism. Fluorescence lifetime imaging (FLIM) to measure receptor proximity; BTK inhibitors; neutrophil activation assays; alveolar neutrophils from ALI/ARDS patients American journal of respiratory cell and molecular biology Medium 23239500
2007 CD300a (IRp60), an ITIM-containing inhibitory receptor, co-ligates with FcγRIIa (CD32A) on neutrophils to inhibit FcγRIIa-mediated signaling selectively without inhibiting TLR4-mediated ROS production. LPS and GM-CSF rapidly upregulate CD300a surface expression by translocation of an intracellular pool to the cell surface. HL-60 differentiation model; neutrophil stimulation with LPS/GM-CSF; co-ligation experiments; ROS production assays; flow cytometry Molecular immunology Medium 17588661
2020 FcRn acts as a CD32a (FcγRIIa) coreceptor: CD32a forms a ternary complex with FcRn under acidic conditions upon IgG1 immune complex binding, particularly for the CD32aH (H131) variant which more avidly forms this complex. Both CD32a variants require FcRn to induce innate and adaptive immune responses to IgG ICs. FcRn blockade decreased inflammation in a rheumatoid arthritis model without reducing circulating autoantibody levels. Co-IP/ternary complex formation assays; primary human and mouse cell activation assays; FcRn-deficient mouse models; RA mouse model with FcRn blockade; CD32aH vs. CD32aR allele comparison Journal of experimental medicine High 32658257
2022 FcγRIIa-Syk signaling is a central pathway mediating platelet hyperactivation in COVID-19. Blocking FcγRIIa-Syk signaling (via antibody neutralization, IgG depletion, or the Syk inhibitor fostamatinib) reversed COVID-19 plasma-induced platelet hyperactivation and prevented platelet aggregation in endothelial microfluidic chambers. COVID-19 patient plasma stimulation of control platelets; antibody-mediated FcγRIIa blockade; IgG depletion; Syk inhibitor fostamatinib; microfluidic endothelial chamber assays; proteomics Frontiers in immunology Medium 35309299
1993 FcγRIIa mRNA is expressed predominantly in megakaryocytic cells (with both transmembrane and non-transmembrane forms in comparable amounts); myelomonocytic cells contain all three FcγRII gene transcripts predominantly FcγRIIa1; B lymphocytes do not express FcγRIIa mRNA. This establishes lineage-specific differential expression of FcγRII genes. Northern blot analysis; reverse transcription-PCR; megakaryocytic, myeloid, and lymphoid cell lines Molecular immunology Medium 8464427
1993 A soluble form of FcγRIIa lacking the transmembrane domain but retaining the cytoplasmic domain is produced by alternative splicing. Soluble FcγRIIa protein is secreted into conditioned medium of HEL cells and detectable by immunoprecipitation with IV.3 antibody. cDNA cloning from HEL cell library; RT-PCR; RNase protection analysis; immunoprecipitation of conditioned medium Experimental hematology Medium 8513871
2006 Human skin-derived mast cells (MC_TC type) constitutively express FcγRIIa (but not FcγRIIb, FcγRI, or FcγRIII) at mRNA and protein levels. FcγRIIa-specific antibody cross-linking triggered mast cell degranulation and secretion of PGD2, LTC4, GM-CSF, IL-5, IL-6, IL-13, and TNF-α in a dose-dependent manner. Microarray; RT-PCR; Western blot; flow cytometry; FcγRIIa-specific mAb cross-linking; mediator release assays (β-hexosaminidase, PGD2, LTC4, cytokines) Journal of immunology High 16785568
1996 Grb2 SH2 domain binds to two tyrosine-phosphorylated proteins (p38 and p63) following FcγRIIa cross-linking in platelets; both are in the particulate fraction and also bind PLCγ1 SH2/SH3 domains. SLP-76 (p75) is tyrosine-phosphorylated and associates with Grb2 SH3 domains along with SOS1 and p120 upon FcγRIIa stimulation. GST-Grb2 fusion protein pull-down; co-immunoprecipitation; tyrosine phosphorylation assays; platelet subcellular fractionation; anti-SLP-76 immunoblot Blood Medium 8695800
1996 The Mac-1 integrin (β2 integrin, CD11b/CD18) but not p150,95 (CD11c/CD18) associates with FcγRIIa on K562 cells. Anti-FcγRII mAb profoundly inhibited Mac-1-mediated cell adhesion but not p150,95-mediated adhesion, indicating a specific functional interaction between FcγRIIa and Mac-1. K562 cell transfection with Mac-1 or p150,95; cell adhesion assays; anti-FcγRII blocking antibodies European journal of immunology Medium 8566068
2018 FcγRIIa-expressing platelets are directly activated by IgG immune complexes in vivo and are sufficient to restore susceptibility to IgG-dependent anaphylaxis. Platelet depletion attenuated anaphylaxis severity, while thrombocythemia worsened it. Serotonin released by FcγRIIa-activated platelets contributed to anaphylaxis severity. Human FcγRIIa transgenic mouse models; platelet depletion/thrombocythemia; in vivo anaphylaxis induction; serotonin measurement; cohort of drug-induced anaphylaxis patients Science immunology High 29654057
2019 Cancer cell-derived IgG directly interacts with platelet FcγRIIa (demonstrated by co-immunoprecipitation) and activates platelets. Blocking FcγRIIa or knocking down cancer cell IgG reduced platelet activation markers (CD62P, PAC-1), aggregation, and ATP release. FcγRIIa downstream signaling (Syk, PLCγ2) was activated. Co-immunoprecipitation of cancer cell IgG with platelet FcγRIIa; flow cytometry (CD62P, PAC-1); platelet aggregation; ATP release; Western blot (Syk, PLCγ2); IgG siRNA knockdown in cancer cells Cell death & disease Medium 30692520
2020 FcγRIIa expression accelerates lupus nephritis and increases platelet activation in SLE. In FCGR2A transgenic NZB/NZWF1 mice, FcγRIIa expression by bone marrow cells severely aggravated lupus nephritis and accelerated death. Circulating platelets were degranulated and interacted with neutrophils, and FcγRIIa led to thrombosis in lungs and kidneys. Platelet transcriptome showed enrichment for type I interferon response genes specifically in FcγRIIa-expressing lupus mice. FcγRIIa transgenic × NZB/NZWF1 SLE mouse model; survival analysis; histopathology; platelet-neutrophil interaction assays; platelet transcriptomics Blood High 33331924
2019 Lupus-associated RNA-containing immune complexes activate human neutrophils to produce ROS and IL-8 via FcγRIIa in a TLR-independent manner. Blocking FcγRIIa inhibited ROS production. RNA-ICs induce Ca2+ flux (unlike TLR7/8 ligands), and TLR7/9 deletion had no effect on IC-induced neutrophil activation. FcγRIIa blocking antibodies; TLR7/TLR9-deficient mouse neutrophils; ROS assays; Ca2+ flux; IL-8 production; chloroquine inhibition Journal of immunology High 30610165
2018 Anti-FcγRIIa antibody VIB9600 suppresses FcγRIIa activation by two mechanisms: blocking ligand engagement and internalizing FcγRIIa from the cell surface. VIB9600 inhibits IC-induced IFN-α from PDCs, ANCA-induced ROS from neutrophils, and IC-induced TNF-α and IL-6; in transgenic mice, it suppressed thrombocytopenia, nephritis, and arthritis. Biacore SPR; confocal microscopy; flow cytometry; cell-based activation assays; FcγRIIa transgenic mouse disease models; NHP PK/PD studies Annals of the rheumatic diseases High 30459279
2015 Hypomethylation of the FCGR2A promoter CpG sites is associated with increased FCGR2A mRNA expression. Reporter gene assays demonstrated that CpG sites in the FCGR2A promoter region are sufficient to modulate gene expression, establishing a direct epigenetic (DNA methylation) mechanism for FCGR2A transcriptional regulation. HumanMethylation27 BeadChip; pyrosequencing validation; reporter gene assays; mRNA expression analysis Arthritis & rheumatology Medium 25470559

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Impact of Fc{gamma}RIIa-Fc{gamma}RIIIa polymorphisms and KRAS mutations on the clinical outcome of patients with metastatic colorectal cancer treated with cetuximab plus irinotecan. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 425 19164213
1996 Fc gamma RIIA alleles are heritable risk factors for lupus nephritis in African Americans. The Journal of clinical investigation 385 8636449
2007 FCGR2A and FCGR3A polymorphisms associated with clinical outcome of epidermal growth factor receptor expressing metastatic colorectal cancer patients treated with single-agent cetuximab. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 384 17704420
2003 Fc gamma RIIa is expressed on natural IFN-alpha-producing cells (plasmacytoid dendritic cells) and is required for the IFN-alpha production induced by apoptotic cells combined with lupus IgG. Journal of immunology (Baltimore, Md. : 1950) 305 12960360
1994 Anti-neutrophil cytoplasmic antibodies engage and activate human neutrophils via Fc gamma RIIa. Journal of immunology (Baltimore, Md. : 1950) 251 8027554
2017 CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses. Nature 195 28297712
2000 C-reactive protein binding to FcgammaRIIa on human monocytes and neutrophils is allele-specific. The Journal of clinical investigation 170 10675363
1999 The role of the human Fc receptor Fc gamma RIIA in the immune clearance of platelets: a transgenic mouse model. Journal of immunology (Baltimore, Md. : 1950) 163 10201963
2003 Fc gamma RIIIa and Fc gamma RIIa polymorphisms do not predict response to rituximab in B-cell chronic lymphocytic leukemia. Blood 158 14563637
2000 The IgG Fc contains distinct Fc receptor (FcR) binding sites: the leukocyte receptors Fc gamma RI and Fc gamma RIIa bind to a region in the Fc distinct from that recognized by neonatal FcR and protein A. Journal of immunology (Baltimore, Md. : 1950) 134 10799893
2009 Copy number variation at the FCGR locus includes FCGR3A, FCGR2C and FCGR3B but not FCGR2A and FCGR2B. Human mutation 131 19309690
2015 Human platelet IgG Fc receptor FcγRIIA in immunity and thrombosis. Journal of thrombosis and haemostasis : JTH 120 25900780
2007 Monoclonal antibodies capable of discriminating the human inhibitory Fcgamma-receptor IIB (CD32B) from the activating Fcgamma-receptor IIA (CD32A): biochemical, biological and functional characterization. Immunology 115 17386079
1993 Differential expression of Fc gamma RIIA, Fc gamma RIIB and Fc gamma RIIC in hematopoietic cells: analysis of transcripts. Molecular immunology 108 8464427
1996 Fc gamma RIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease. Clinical and experimental immunology 100 8625518
1995 Identification of signaling motifs within human Fc gamma RIIa and Fc gamma RIIb isoforms. Blood 100 7718892
2015 The platelet Fc receptor, FcγRIIa. Immunological reviews 99 26497525
1997 Fc gamma RIIA H/R 131 polymorphism, subclass-specific IgG anti-heparin/platelet factor 4 antibodies and clinical course in patients with heparin-induced thrombocytopenia and thrombosis. Blood 99 9002937
2006 Fc gamma RIIa, not Fc gamma RIIb, is constitutively and functionally expressed on skin-derived human mast cells. Journal of immunology (Baltimore, Md. : 1950) 96 16785568
2017 Association of Polymorphisms in FCGR2A and FCGR3A With Degree of Trastuzumab Benefit in the Adjuvant Treatment of ERBB2/HER2-Positive Breast Cancer: Analysis of the NSABP B-31 Trial. JAMA oncology 92 27812689
2003 Signaling role for phospholipase C gamma 2 in platelet glycoprotein Ib alpha calcium flux and cytoskeletal reorganization. Involvement of a pathway distinct from FcR gamma chain and Fc gamma RIIA. The Journal of biological chemistry 92 12813055
2013 A novel and essential role for FcγRIIa in cancer cell-induced platelet activation. Blood 88 24258815
1996 Rapid detection of the Fc gamma RIIA-H/R 131 ligand-binding polymorphism using an allele-specific restriction enzyme digestion (ASRED). Journal of immunological methods 85 8960098
2014 Shifting FcγRIIA-ITAM from activation to inhibitory configuration ameliorates arthritis. The Journal of clinical investigation 81 25061875
2014 Platelet 12-LOX is essential for FcγRIIa-mediated platelet activation. Blood 81 25100742
2005 Analysis of binding sites in human C-reactive protein for Fc{gamma}RI, Fc{gamma}RIIA, and C1q by site-directed mutagenesis. The Journal of biological chemistry 79 15878871
2003 Phosphorylation of FcgammaRIIA is required for the receptor-induced actin rearrangement and capping: the role of membrane rafts. Journal of cell science 78 12508114
1995 Function of human Fc gamma RIIA and Fc gamma RIIIB. Seminars in immunology 78 7612894
1997 Antibodies to C1q in systemic lupus erythematosus: characteristics and relation to Fc gamma RIIA alleles. Kidney international 77 9350662
1994 Substitutions and deletions in the cytoplasmic domain of the phagocytic receptor Fc gamma RIIA: effect on receptor tyrosine phosphorylation and phagocytosis. Blood 77 7521687
1992 Human low-affinity IgG receptor Fc gamma RIIa (CD32) introduced into mouse fibroblasts mediates phagocytosis of sensitized erythrocytes. Blood 75 1532752
2018 Platelets expressing IgG receptor FcγRIIA/CD32A determine the severity of experimental anaphylaxis. Science immunology 66 29654057
2007 The CD300a (IRp60) inhibitory receptor is rapidly up-regulated on human neutrophils in response to inflammatory stimuli and modulates CD32a (FcgammaRIIa) mediated signaling. Molecular immunology 65 17588661
1993 Mapping epitopes of human Fc gamma RII (CDw32) with monoclonal antibodies and recombinant receptors. Journal of immunology (Baltimore, Md. : 1950) 60 7679695
1994 Correlations among tyrosine phosphorylation of Shc, p72syk, PLC-gamma 1, and [Ca2+]i flux in Fc gamma RIIA signaling. Journal of immunology (Baltimore, Md. : 1950) 59 8144900
2006 Platelet FcgammaRIIA binds and internalizes IgG-containing complexes. Experimental hematology 58 17046568
2017 Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases. The Journal of clinical investigation 57 28891817
2015 Identification of an association between genomic hypomethylation of FCGR2A and susceptibility to Kawasaki disease and intravenous immunoglobulin resistance by DNA methylation array. Arthritis & rheumatology (Hoboken, N.J.) 57 25470559
2013 Correlation of HER2, FCGR2A, and FCGR3A gene polymorphisms with trastuzumab related cardiac toxicity and efficacy in a subgroup of patients from UNICANCER-PACS 04 trial. Breast cancer research and treatment 57 23780683
2022 Signaling Through FcγRIIA and the C5a-C5aR Pathway Mediate Platelet Hyperactivation in COVID-19. Frontiers in immunology 54 35309299
2000 Cell-specific, activation-dependent regulation of neutrophil CD32A ligand-binding function. Blood 53 10648424
2009 Eptifibatide-induced thrombocytopenia and thrombosis in humans require FcgammaRIIa and the integrin beta3 cytoplasmic domain. The Journal of clinical investigation 50 19197137
2020 The Fully human anti-CD47 antibody SRF231 exerts dual-mechanism antitumor activity via engagement of the activating receptor CD32a. Journal for immunotherapy of cancer 49 32345627
2020 FcγRIIA expression accelerates nephritis and increases platelet activation in systemic lupus erythematosus. Blood 49 33331924
2015 Anti-miR-148a regulates platelet FcγRIIA signaling and decreases thrombosis in vivo in mice. Blood 49 26516227
1990 Different isoforms of human FcRII distinguished by CDw32 antibodies. Journal of immunology (Baltimore, Md. : 1950) 49 2138195
2019 Oral Bruton tyrosine kinase inhibitors block activation of the platelet Fc receptor CD32a (FcγRIIA): a new option in HIT? Blood advances 48 31809536
2016 Neuroblastoma patients with high-affinity FCGR2A, -3A and stimulatory KIR 2DS2 treated by long-term infusion of anti-GD2 antibody ch14.18/CHO show higher ADCC levels and improved event-free survival. Oncoimmunology 48 27999754
2004 The role of FcgammaRIIA and IIIA polymorphisms in autoimmune diseases. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 48 15194164
2001 Signal transduction by human-restricted Fc gamma RIIa involves three distinct cytoplasmic kinase families leading to phagocytosis. Journal of immunology (Baltimore, Md. : 1950) 48 11441091
2019 Cancer cell-derived immunoglobulin G activates platelets by binding to platelet FcγRIIa. Cell death & disease 47 30692520
2002 C-reactive protein induces signaling through Fc gamma RIIa on HL-60 granulocytes. Journal of immunology (Baltimore, Md. : 1950) 47 11801683
1997 Fc gamma RIIa polymorphism in systemic lupus erythematosus. Annals of the rheumatic diseases 47 9496155
2021 Platelet FcγRIIA in immunity and thrombosis: Adaptive immunothrombosis. Journal of thrombosis and haemostasis : JTH 46 33587783
2006 Association of FCGR2A and FCGR2A-FCGR3A haplotypes with susceptibility to giant cell arteritis. Arthritis research & therapy 46 16846526
2003 The protein-tyrosine phosphatase SHP-1 associates with the phosphorylated immunoreceptor tyrosine-based activation motif of Fc gamma RIIa to modulate signaling events in myeloid cells. The Journal of biological chemistry 45 12832410
1996 Characterization of Grb2-binding proteins in human platelets activated by Fc gamma RIIA cross-linking. Blood 44 8695800
2009 Association of FcgammaRIIa (CD32a) with lipid rafts regulates ligand binding activity. Journal of immunology (Baltimore, Md. : 1950) 43 19494328
2020 FcRn is a CD32a coreceptor that determines susceptibility to IgG immune complex-driven autoimmunity. The Journal of experimental medicine 42 32658257
2018 FCGR2A/FCGR3A Gene Polymorphisms and Clinical Variables as Predictors of Response to Tocilizumab and Rituximab in Patients With Rheumatoid Arthritis. Journal of clinical pharmacology 42 30457672
2000 Thrombosis and shock induced by activating antiplatelet antibodies in human Fc gamma RIIA transgenic mice: the interplay among antibody, spleen, and Fc receptor. Blood 41 11110699
1995 Role of Fc gamma RIIA gene polymorphism in human platelet activation by monoclonal antibodies. Thrombosis and haemostasis 40 8772237
2009 Dynamics of the interaction of human IgG subtype immune complexes with cells expressing R and H allelic forms of a low-affinity Fc gamma receptor CD32A. Journal of immunology (Baltimore, Md. : 1950) 39 20007585
1993 A soluble form of the human Fc receptor Fc gamma RIIA: cloning, transcript analysis and detection. Experimental hematology 39 8513871
1989 Human basophils selectively express the Fc gamma RII (CDw32) subtype of IgG receptor. The Journal of allergy and clinical immunology 38 2532230
2015 Variation at FCGR2A and functionally related genes is associated with the response to anti-TNF therapy in rheumatoid arthritis. PloS one 36 25848939
2019 In vitro elimination of epidermal growth factor receptor-overexpressing cancer cells by CD32A-chimeric receptor T cells in combination with cetuximab or panitumumab. International journal of cancer 35 31479522
2003 Physical proximity and functional interplay of PECAM-1 with the Fc receptor Fc gamma RIIa on the platelet plasma membrane. Blood 35 12893767
2005 Polymorphism of Fc gamma RIIa may affect the efficacy of gamma-globulin therapy in Kawasaki disease. Journal of clinical immunology 34 16133986
2003 Signal sequence within Fc gamma RIIA controls calcium wave propagation patterns: apparent role in phagolysosome fusion. Proceedings of the National Academy of Sciences of the United States of America 34 12676989
1993 Expression of the Fc receptor for IgG (Fc gamma RII/CDw32) by human circulating T and B lymphocytes. Journal of immunology (Baltimore, Md. : 1950) 34 8496609
2014 A genetic variant rs1801274 in FCGR2A as a potential risk marker for Kawasaki disease: a case-control study and meta-analysis. PloS one 33 25093412
1995 The low affinity Fc gamma RIIa and Fc gamma RIIIb on polymorphonuclear neutrophils are differentially regulated by CD45 phosphatase. Journal of immunology (Baltimore, Md. : 1950) 33 7561111
2014 FCGR2A and FCGR3A polymorphisms and clinical outcome in metastatic colorectal cancer patients treated with first-line 5-fluorouracil/folinic acid and oxaliplatin +/- cetuximab. BMC cancer 31 24884501
2001 Simultaneous engagement of thrombin and Fc gamma RIIA receptors results in platelets expressing high levels of procoagulant proteins. The Journal of laboratory and clinical medicine 31 11753286
1993 Fc gamma RIIA-mediated phagocytosis and receptor phosphorylation in cells deficient in the protein tyrosine kinase Src. Experimental hematology 31 8405229
2019 FCGR3A and FCGR2A Genotypes Differentially Impact Allograft Rejection and Patients' Survival After Lung Transplant. Frontiers in immunology 30 31249568
2006 Alteration of the Fc gamma RIIa dimer interface affects receptor signaling but not ligand binding. Journal of immunology (Baltimore, Md. : 1950) 30 16751395
1999 Biochemical analysis and crystallisation of Fc gamma RIIa, the low affinity receptor for IgG. Immunology letters 30 10397151
2017 Male-specific association of the FCGR2A His167Arg polymorphism with Kawasaki disease. PloS one 29 28886140
2016 Associations between PTPRC rs10919563 A/G and FCGR2A R131H polymorphisms and responsiveness to TNF blockers in rheumatoid arthritis: a meta-analysis. Rheumatology international 29 27074847
2012 FCGR2A/CD32A and FCGR3A/CD16A variants and EULAR response to tumor necrosis factor-α blockers in psoriatic arthritis: a longitudinal study with 6 months of followup. The Journal of rheumatology 28 22467926
2004 Recruitment of the cross-linked opsonic receptor CD32A (FcgammaRIIA) to high-density detergent-resistant membrane domains in human neutrophils. The Biochemical journal 28 15130090
2002 Early events in the activation of Fc gamma RIIA in human neutrophils: stimulated insolubilization, translocation to detergent-resistant domains, and degradation of Fc gamma RIIA. Journal of immunology (Baltimore, Md. : 1950) 28 11937562
2018 Humanised effector-null FcγRIIA antibody inhibits immune complex-mediated proinflammatory responses. Annals of the rheumatic diseases 27 30459279
2012 Bruton's tyrosine kinase mediates FcγRIIa/Toll-like receptor-4 receptor crosstalk in human neutrophils. American journal of respiratory cell and molecular biology 27 23239500
2010 Divergent intracellular sorting of Fc{gamma}RIIA and Fc{gamma}RIIB2. The Journal of biological chemistry 27 20736173
2006 Anti-OxLDL IgG blocks OxLDL interaction with CD36, but promotes FcgammaR, CD32A-dependent inflammatory cell adhesion. Immunology letters 27 17081622
1996 The beta 2 integrin Mac-1 but not p150,95 associates with Fc gamma RIIA. European journal of immunology 27 8566068
2016 Fc Gamma Receptor IIA (CD32A) R131 Polymorphism as a Marker of Genetic Susceptibility to Sepsis. Inflammation 26 26490967
2010 Analysis of MIF, FCGR2A and FCGR3A gene polymorphisms with susceptibility to pulmonary tuberculosis in Moroccan population. Journal of genetics and genomics = Yi chuan xue bao 26 20439102
2007 Genetic linkage of Fc gamma RIIa and Fc gamma RIIIa and implications for their use in predicting clinical responses to CD20-directed monoclonal antibody therapy. Clinical lymphoma & myeloma 25 17324336
2004 Fc gamma RIIa polymorphism: a susceptibility factor for immune complex-mediated lupus nephritis in Brazilian patients. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 24 15004265
1998 A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor. Blood 24 9427722
2019 Lupus-Associated Immune Complexes Activate Human Neutrophils in an FcγRIIA-Dependent but TLR-Independent Response. Journal of immunology (Baltimore, Md. : 1950) 23 30610165
2016 Association of FCGR2A rs1801274 polymorphism with susceptibility to autoimmune diseases: A meta-analysis. Oncotarget 23 27270653
1994 CD31 (PECAM-1), CDw32 (Fc gamma RII), and anti-HLA class I monoclonal antibodies recognize phosphotyrosine-containing proteins on the surface of human neutrophils. Journal of immunology (Baltimore, Md. : 1950) 23 7515918
1993 Detection and quantification of secreted soluble Fc gamma RIIA in human sera by an enzyme-linked immunosorbent assay. Journal of immunological methods 22 8228278
2017 The influence of FCGR2A and FCGR3A polymorphisms on the survival of patients with recurrent or metastatic squamous cell head and neck cancer treated with cetuximab. The pharmacogenomics journal 21 28719596
2015 FCGR2A, FCGR3A, FCGR3B polymorphisms and susceptibility to rheumatoid arthritis: a meta-analysis. Clinical and experimental rheumatology 21 26314337

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