Affinage

Showing FCGR1A — FCGR1 is a alias.

FCGR1A

High affinity immunoglobulin gamma Fc receptor I · UniProt P12314

Length
374 aa
Mass
42.6 kDa
Annotated
2026-06-09
100 papers in source corpus 35 papers cited in narrative 35 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FCGR1A (Fcγ RI, CD64) is the high-affinity IgG Fc receptor that drives antibody-dependent effector functions of myeloid cells, including phagocytosis, ADCC, antigen presentation, and proinflammatory cytokine output (PMID:11911824, PMID:11911823). High-affinity, IgG-subclass-specific binding is conferred by the receptor's extracellular domains 2 and 3, with domain 1 supporting conformational stability and a domain-3 receptor-glycan contact contributing to affinity (PMID:9881694, PMID:26497521). The α-chain itself lacks signaling motifs: phagocytosis, ADCC, and enhancement of immune-complex viral infectivity all require an ITAM supplied in trans by the associated FcR γ-chain (or, in its absence, by Fcγ RIIa), and abrogating that ITAM uncouples signaling from receptor engagement (PMID:7516890, PMID:9737671, PMID:15075346, PMID:17005690). The α-chain cytoplasmic tail carries an autonomous, γ-chain-independent function: it is constitutively serine-phosphorylated, sets the kinetics of endocytosis/phagocytosis and the calcium dependence and cytokine specificity of responses (notably IL-6 secretion), and routes internalized antigen to MHC class II late-endosomal compartments — activities mediated in part through a selective interaction with periplakin (PMID:10397749, PMID:10514529, PMID:12200451, PMID:15229321, PMID:15161926). Downstream of aggregation, Fcγ RI signals through a phospholipase D1→sphingosine kinase-1 cascade distinct from the PLCγ1 pathway of Fcγ RIIa, recruits PKC isoenzymes in a differentiation-state-dependent manner, and drives NF-κB-regulated NLRP3 inflammasome activation and IL-1β/IL-18 release (PMID:10233728, PMID:19420354, PMID:29920250). The receptor resides constitutively in lipid rafts and organizes into nanoclusters whose immune-complex avidity is tuned by cytokine-driven, actin-dependent 'inside-out' signaling (regulated by PP1) and whose proximity to inhibitory SIRPα nanoclusters reorganizes upon activation (PMID:18207250, PMID:28289091, PMID:30042128). C-reactive protein is a non-IgG ligand that binds the Fcγ RI extracellular region with affinity strongly enhanced by the γ-chain, triggering phagocytosis and PLD activation (PMID:12383205, PMID:17255341). Beyond myeloid cells, Fcγ RI in sensory neurons cell-autonomously mediates IgG immune-complex-induced joint pain and CRP-driven neuropathic pain (PMID:31211699, PMID:36727833). Coding and regulatory FCGR1A variants modulate CD64 expression and effector function (PMID:35371020).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1994 High

    Established that Fcγ RI lacks intrinsic signaling capacity and depends on an associated subunit, answering how a receptor with a short tail triggers phagocytosis.

    Evidence COS-1 reconstitution of wild-type and cytoplasmic-deletion Fcγ RI with the Fcγ RIIIA γ-subunit plus tyrosine kinase inhibitor studies

    PMID:7516890

    Open questions at the time
    • Did not define the γ-chain ITAM tyrosines required
    • Phagocytosis assayed in a non-myeloid heterologous cell line
  2. 1996 High

    Mapped expression and IgG-affinity determinants to the extracellular region and showed conserved γ-chain association across species, framing the structural basis of high-affinity binding.

    Evidence Kinetic binding analysis of NOD vs BALB/c Fcγ RI, COS-7 extracellular domain-swap chimeras, and co-transfection with the Fcε RI γ-subunit

    PMID:8663283

    Open questions at the time
    • Mouse receptor; human affinity determinants inferred
    • Mechanism linking extracellular mutations to surface expression unresolved
  3. 1998 High

    Defined that an intact ITAM in either the γ-chain or Fcγ RIIa is essential for triggering phagocytosis and ADCC, and that extracellular domains 2/3 confer high-affinity subclass-specific binding.

    Evidence ITAM mutagenesis and reconstitution in IIA1.6 cells with phagocytosis/ADCC readouts; domain-swap chimeras with monomeric IgG binding

    PMID:9737671 PMID:9881694

    Open questions at the time
    • Did not resolve which kinases read the ITAM
    • Domain-3 glycan contribution not yet identified
  4. 1999 High

    Resolved an autonomous, γ-chain-independent role for the α-chain cytoplasmic tail in trafficking and cytokine specificity, distinguishing it from the ITAM-driven phagocytic signal.

    Evidence IIA1.6 and macrophage transfectants with tail-deletion and ITAM-mutant constructs, immunoelectron microscopy, MHC-II antigen presentation, calcium and cytokine assays; PKC isoenzyme fractionation in differentiated U937 cells

    PMID:10233728 PMID:10397749 PMID:10514529

    Open questions at the time
    • Trafficking motifs within the tail not pinpointed
    • Link between PKC isoenzyme usage and downstream phospholipases not directly tested
  5. 2002 High

    Established constitutive serine phosphorylation of the α-chain tail as a regulatory layer and demonstrated the receptor's non-redundant in vivo roles in effector function and antibody control.

    Evidence Serine→alanine and truncation mutants in P388D1 macrophages with okadaic acid; Fcγ RI knockout mice across hypersensitivity, arthritis, and infection models; CRP direct binding by SPR and functional phagocytosis/PLD assays

    PMID:11911823 PMID:11911824 PMID:12200451 PMID:12383205

    Open questions at the time
    • Serine kinase(s) acting on the tail not identified
    • CRP versus IgG binding-site overlap on the receptor unresolved
  6. 2004 High

    Identified periplakin as a selective α-chain cytoplasmic-tail partner controlling ligand binding and trafficking, and dissected receptor-proximal kinase differences from Fcγ RIIa.

    Evidence Reciprocal co-IP, blot-overlay, alanine-scanning and TAT-peptide interference for periplakin; Syk/Hck/Lyn co-IP and γ-chain-independent Fcγ RIIa-ITAM phagocytosis in COS cells

    PMID:15075346 PMID:15136586 PMID:15161926 PMID:15229321

    Open questions at the time
    • How periplakin mechanistically alters ligand-binding capacity unclear
    • Functional significance of weaker Syk recruitment in primary myeloid cells not established
  7. 2006 High

    Showed that Fcγ RI signaling competency (γ-chain ITAM) is required for antibody-dependent enhancement of dengue infectivity, extending its functional repertoire beyond simple uptake.

    Evidence Site-directed ITAM mutagenesis in COS-7 with dengue plaque and flow-cytometric infectivity readouts versus Fcγ RIIa

    PMID:17005690

    Open questions at the time
    • Signaling step coupling ITAM to enhanced viral entry unresolved
    • Heterologous cell system may not reflect primary monocytes
  8. 2007 Medium

    Quantified γ-chain enhancement of CRP binding (~30-fold), revealing a transmembrane contribution to non-IgG ligand engagement.

    Evidence Single-molecule confocal binding kinetics in COS-7 cells expressing Fcγ RI alone or with γ-chain

    PMID:17255341

    Open questions at the time
    • Structural basis of γ-chain transmembrane contribution not defined
    • Single lab, heterologous cells
  9. 2008 Medium

    Localized Fcγ RI to lipid rafts and demonstrated a soluble receptor decoy strategy, addressing membrane organization and therapeutic potential.

    Evidence Detergent-insoluble membrane fractionation and GM1 co-patching; recombinant soluble Fcγ RIA SPR binding plus mast-cell cytokine, Arthus, and arthritis models

    PMID:18097060 PMID:18207250

    Open questions at the time
    • Functional consequence of raft residence for signaling not fully defined
    • Decoy efficacy translation to human disease untested
  10. 2009 High

    Defined a Fcγ RI-specific PLD1→sphingosine kinase-1 signaling axis driving inflammatory mediators and MHC-II trafficking, distinct from Fcγ RIIa's PLCγ1 pathway.

    Evidence Pharmacological PLD1/SK1 inhibition, HLA-DM compartment co-localization, cytokine and antigen-presentation assays in U937 cells and primary human monocytes

    PMID:19420354

    Open questions at the time
    • Connection between γ-chain ITAM and PLD1 activation not mapped
    • Inhibitor-based pathway dissection lacks genetic confirmation
  11. 2010 High

    Revealed an IgG-independent role of the α-chain cytoplasmic tail in bacterial OmpA recognition and identified Fcγ RI as a control point in fibrocyte differentiation, broadening its ligand and effector scope.

    Evidence Fcγ RIa knockout mice in E. coli K1 meningitis with tail-truncation, γ-chain recruitment co-IP, phosphorylation analysis, and adoptive transfer; Fcγ RI KO/siRNA in SAP-driven fibrocyte differentiation assays

    PMID:21124939 PMID:22493081

    Open questions at the time
    • Signaling pathway downstream of OmpA-induced phosphorylation undefined
    • SAP-Fcγ RI binding interface not characterized
  12. 2012 Medium

    Linked Fcγ RI activation to NF-κB-dependent NLRP3 inflammasome assembly and IL-1β/IL-18 release, connecting the receptor to inflammasome biology.

    Evidence Gain-of-function in Ba/F3 cells with PDTC inhibition and siRNA knockdown in THP-1 macrophages with inflammasome protein and cytokine readouts

    PMID:29920250

    Open questions at the time
    • Intermediate signaling between Fcγ RI and NF-κB not mapped
    • Single lab
  13. 2015 Medium

    Provided structural and signaling-context detail: a crystal structure of the IgG-Fc complex implicating a domain-3 glycan contact, and a model of monomeric-IgG tonic signaling versus immune-complex activation.

    Evidence Crystallography of the Fcγ RI–IgG-Fc complex (reported in review); review synthesis of tonic signaling and IFN-γ/TLR4 crosstalk experiments

    PMID:26497519 PMID:26497521

    Open questions at the time
    • Structural data reported within a review without independent validation here
    • Tonic-signaling mechanism summarized rather than directly demonstrated
  14. 2016 Medium

    Used phosphoproteomics to define the tyrosine-phosphorylation network required for Fcγ RI endocytosis/phagocytosis and showed inhibitory LILRB4 co-ligation dephosphorylates it.

    Evidence Fcγ RI/LILRB4 ligation in THP-1 cells with anti-phosphotyrosine IP, mass spectrometry, and phagocytosis assay

    PMID:27725776

    Open questions at the time
    • Direct substrates of LILRB4-recruited phosphatase not pinpointed
    • Single lab
  15. 2018 High

    Demonstrated cytokine-driven, actin- and PP1-dependent 'inside-out' nanoclustering as the mechanism by which Fcγ RI avidity for immune complexes is dynamically tuned, with functional consequences for ADCC.

    Evidence Super-resolution single-particle tracking, PP1 inhibition (calyculin A), actin disruption, cytokine priming, and CD20+ tumor ADCC assay

    PMID:30042128

    Open questions at the time
    • How PP1 controls clustering without altering receptor phosphorylation unresolved
    • Identity of clustering scaffold proteins not defined
  16. 2017 High

    Resolved spatial integration of activating and inhibitory signals by imaging constitutive Fcγ RI–SIRPα nanocluster association and their activation-dependent segregation.

    Evidence Dual-color dSTORM super-resolution imaging with Src-family kinase inhibition, CD47-SIRPα co-ligation, and actin disruption

    PMID:28289091

    Open questions at the time
    • Molecular tether linking the two nanocluster types not identified
    • Functional output of concentric-ring reorganization not quantified
  17. 2019 High

    Established a cell-autonomous neuronal function for Fcγ RI in sensory neurons, mediating IgG immune-complex-induced joint pain independent of inflammation.

    Evidence Global and sensory-neuron-specific Fcgr1 knockout mice with electrophysiology and pain behavioral assays in immune-complex and arthritis models

    PMID:31211699

    Open questions at the time
    • Downstream neuronal signaling and ion-channel coupling undefined
    • Whether γ-chain participates in neurons not addressed
  18. 2019 High

    Showed that Fcγ RI-mediated IgG sequestration in immune cells drives hepatic off-target uptake of radioimmunoconjugates, a pharmacological consequence of high-affinity Fc binding.

    Evidence SPR, ELISA, flow cytometry, and PET biodistribution of glycosylated vs deglycosylated conjugates in athymic, NSG, and humanized NSG mice

    PMID:30733320

    Open questions at the time
    • Cellular site of hepatic sequestration not fully resolved
    • Relevance to fully human contexts inferred from humanized mice
  19. 2021 Medium

    Demonstrated that Fcγ RI expression dramatically potentiates antibody neutralization of HIV-1, indicating a role for the receptor in antiviral antibody function.

    Evidence Neutralization assays in TZM-bl cells with/without Fcγ RI, tier-1/tier-2 virus comparison, and guinea pig immune sera with Fcγ RI-blocking controls

    PMID:33431684

    Open questions at the time
    • Mechanism of potentiation (capture vs signaling) not dissected
    • Single lab, cell-based
  20. 2022 Medium

    Linked FCGR1A genetic variation to CD64 expression and effector function, providing human genetic evidence for functional modulation.

    Evidence Promoter reporter assays and genotype-phenotype association plus phagocytosis/degranulation/cytokine assays for the p.D324N coding variant

    PMID:35371020

    Open questions at the time
    • Mechanism by which p.D324N alters function not defined
    • Variant effects on clinical phenotypes not established
  21. 2023 High

    Separated the IgG-capture function from intracellular signaling and extended neuronal Fcγ RI to neuropathic pain, clarifying both engineering applications and pain mechanisms.

    Evidence Full-length vs intracellularly truncated CD64 overexpression in iPSC-derived cells with ADCC/CDC and humanized mouse models; DRG-neuron-specific Fcgr1 conditional knockout with CRP/IgG microinjection and pain behavior

    PMID:36593395 PMID:36727833

    Open questions at the time
    • Neuronal Fcγ RI signaling effectors not fully mapped
    • Whether neuronal CRP signaling uses the γ-chain unresolved
  22. 2025 Medium

    Showed therapeutic antibody Fc engagement of CD64 can mediate cytokine capture and internalization, demonstrating an Fc-CD64 axis exploitable for drug potency.

    Evidence Flow cytometry, live-cell confocal imaging of IL-23 internalization, and CD64+ THP-1 co-culture reporter assays with Fc-blocking controls (guselkumab vs risankizumab)

    PMID:40145093

    Open questions at the time
    • In vitro only; in vivo relevance untested
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the α-chain cytoplasmic tail, serine phosphorylation, periplakin, and the γ-chain ITAM are mechanistically integrated to specify divergent outcomes (phagocytosis vs antigen routing vs cytokine programs vs neuronal pain) remains unresolved.
  • No unified signaling model connecting tail phosphorylation to PLD1/SK1 and inflammasome outputs
  • Neuronal Fcγ RI downstream effectors and γ-chain dependence undefined
  • Structural basis of nanocluster scaffolding and SIRPα tethering unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 3 GO:0060089 molecular transducer activity 3 GO:0001618 virus receptor activity 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005768 endosome 2
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3 R-HSA-5653656 Vesicle-mediated transport 3
Partners
CRPFCER1GFCGR2ALILRB4PPLSIRPASYK
Complex memberships
Fcγ RI α-chain / FcR γ-chain complex

Evidence

Reading pass · 35 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 FcγRI (CD64) does not require its own cytoplasmic domain to mediate phagocytosis; instead, the γ-subunit of FcγRIIIA confers phagocytic function to FcγRI. Coexpression of FcγRI with the FcγRIIIA γ-subunit in COS-1 cells conferred phagocytic capability even to a cytoplasmic-domain-deleted mutant of FcγRI, demonstrating that the γ-subunit ITAM, not the FcγRI cytoplasmic tail, drives the phagocytic signal. COS-1 cell transfection with wild-type and cytoplasmic-domain-deletion mutants of FcγRI; co-transfection with γ-subunit of FcγRIIIA; IgG-coated red blood cell phagocytosis assay; tyrosine kinase inhibitor (tyrphostin 23) studies Experimental hematology High 7516890
1996 Extracellular domain mutations in the NOD mouse FcγRI increase IgG affinity ~10-fold (via a profoundly reduced dissociation rate) while reducing surface expression to one-tenth of wild-type. The expression level differences map to the extracellular region, and mouse FcγRI can associate with the FcεRI γ-subunit analogously to human FcγRI. Kinetic binding analysis (association/dissociation rates) of NOD vs BALB/c FcγRI; COS-7 transfection with chimeric extracellular domain swaps; co-transfection with FcεRI γ-subunit The Journal of biological chemistry High 8663283
1998 FcγRIa-γ-chain complexes expressed in IIA1.6 cells trigger both phagocytosis and ADCC, and an intact ITAM in either the FcR γ-chain or FcγRIIa is essential for triggering these biological functions via the FcγRIa complex. Transfection of FcγRIa and γ-chain constructs into IIA1.6 cells; ITAM mutagenesis; phagocytosis of Staphylococcus aureus; ADCC of erythrocytes Clinical and experimental immunology High 9737671
1998 The unique high-affinity IgG2a binding of FcγRI (CD64) is conferred by the specific interaction between extracellular domains 2 and 3; domain 1 plays a supporting role in conformational stability. Replacement of domains 2 and 3 of FcγRII with those of FcγRI reconstitutes specific high-affinity monomeric IgG2a binding. Domain-swap chimeric receptors generated between mouse FcγRI and mouse FcγRII; IgG binding studies with monomeric IgG2a, IgG1, and IgG2b Molecular immunology High 9881694
1999 The FcγRIa α-chain cytoplasmic tail contains autonomous targeting information directing internalized receptor-antigen complexes to MHC class II-containing late endosomes for antigen presentation, independently of the FcR γ-chain ITAM. Deletion of the cytoplasmic tail diverts complexes to the recycling pathway and decreases antigen presentation, demonstrating a functional role for the tail distinct from canonical tyrosine/dileucine motifs. IIA1.6 cell transfection with FcγRIa constructs (wild-type, ITAM-mutant γ-chain, cytoplasmic-tail deletion); immunoelectron microscopy tracking receptor-ligand complex trafficking; MHC class II antigen presentation assay Blood High 10397749
1999 The cytoplasmic domain (CY) of FcγRIa α-chain directly modulates the functional properties of the receptor complex: CY deletion slows kinetics of receptor-specific phagocytosis and endocytosis, converts calcium-independent phagocytosis to calcium-dependent phagocytosis, and abrogates FcγRIa-specific IL-6 secretion without affecting IL-1β production. Stable transfectants in murine macrophages expressing full-length or CY-deletion mutant FcγRIa; IgG-opsonized particle phagocytosis assay; calcium measurement; cytokine ELISA The Journal of biological chemistry High 10514529
1999 FcγRI aggregation in IFN-γ-primed U937 cells activates the novel PKC isoenzymes δ, ε, and atypical PKC ζ (calcium-independent), whereas in cells differentiated to a macrophage phenotype it activates conventional calcium-dependent PKCs α, β, and γ, consistent with differentiation-state-dependent coupling to distinct phospholipase pathways. PKC activity assays and translocation studies in IFN-γ-primed vs dbcAMP-differentiated U937 cells after FcγRI aggregation; isoenzyme-specific fractionation Immunology Medium 10233728
2002 The serine residues in the FcγRIa α-chain cytoplasmic domain are constitutively phosphorylated and this phosphorylation regulates early tyrosine-phosphorylation cascades and phagocytosis; mutation of cytoplasmic serine residues to alanine abolishes okadaic acid (phosphatase inhibitor) inhibition of phagocytosis, while cytoplasmic domain truncation and serine mutations have distinct effects on cytokine production vs. phagocytosis. FcγRIa molecular variants (serine→alanine mutants, truncation mutants) expressed in murine macrophage P388D1 cells; okadaic acid treatment; phagocytosis assay; tyrosine phosphorylation immunoblot The Journal of biological chemistry High 12200451
2002 FcγRI is required for IgG2a immune complex-induced phagocytosis, cytokine release, cellular cytotoxicity, and antigen presentation in vivo; FcγRI-deficient mice show impaired hypersensitivity responses, reduced cartilage destruction in arthritis, and impaired protection from bacterial infection. FcγRI knockout mouse studies across multiple in vivo models (hypersensitivity, collagen-induced arthritis, bacterial infection); comparison with FcγRIII-KO and complement-deficient mice Immunity High 11911823 11911824
2002 FcγRI is the primary mediator of endocytosis of monomeric IgG; in its absence, kinetics and extent of immune complex phagocytosis are impaired, macrophage-based ADCC is impaired, and immune complex-dependent antigen presentation to T cells is reduced. FcγRI-deficient mice also show elevated antibody responses, implying FcγRI acts as a control point for antibody production. Additionally, FcR-γ-chain-deficient mice express a partially functional FcγRI. FcγRI knockout mouse generation (gene targeting); in vitro phagocytosis, ADCC, and antigen-presentation assays; in vivo antibody response measurements Immunity High 11911823
2002 C-reactive protein (CRP) binds directly to the extracellular portion of FcγRI with approximately 3-fold higher affinity than IgG (KD ≈ 0.81 nM) in a calcium-dependent manner. CRP opsonization of phosphorylcholine-coated erythrocytes induces phagocytosis via FcγRI/γ-chain transfectants and activates phospholipase D in IFN-γ-treated U937 cells, indicating CRP can crosslink FcγRI to trigger signaling. BIAcore surface plasmon resonance for binding kinetics; COS-7 transfection with FcγRI chimeras; phagocytosis assay; phospholipase D activation in U937 cells; IgG1 competition and calcium chelation experiments Immunology High 12383205
2004 Periplakin (PPL) selectively interacts with the intracellular cytoplasmic tail of the FcγRI α-chain (but not other activatory FcRs). This interaction controls FcγRI ligand binding capacity, endocytosis, and antigen presentation; PPL and FcγRI co-localize at the plasma membrane of monocytes, and both are upregulated by IFN-γ. Co-immunoprecipitation; blot-overlay assay; confocal co-localization in monocytes and transfectants; overexpression of C-terminal PPL to assess FcγRI functional outcomes (ligand binding, endocytosis, antigen presentation) Proceedings of the National Academy of Sciences of the United States of America High 15229321
2004 TAT-peptides that block FcγRI–periplakin interaction modulate FcγRI ligand-binding capacity (assessed by erythrocyte-antibody rosetting), demonstrating a dominant-negative role for C-terminal periplakin in FcγRI biological activity. Alanine-substitution mapping of the FcγRI cytoplasmic tail and random mutagenesis of periplakin defined the specific interaction domains. Truncated and alanine-substituted FcγRI mutants; randomly mutagenized periplakin; TAT-peptide blocking of endogenous FcγRI–periplakin interaction; erythrocyte-antibody rosetting assay The Journal of biological chemistry High 15161926
2004 FcγRI can use FcγRIIa (R131 or H131 allele) to phagocytose IgG- or CRP-opsonized erythrocytes in the absence of the FcR γ-chain; this phagocytosis requires the cytoplasmic ITAM of FcγRIIa (mutation of Y205 or cytoplasmic truncation abrogates phagocytosis). COS-7 cells expressing FcγRI or FcγRIIa alone do not phagocytose. COS-7 transfection with FcγRI alone, FcγRIIa alone, or co-transfection; ITAM-mutant FcγRIIa (Y205 mutation and cytoplasmic truncation); erythrocyte phagocytosis assay; CRP and IgG opsonization Journal of leukocyte biology High 15075346
2004 FcγRI and FcγRIIa differ in their interaction with Syk kinase: FcγRIIA interacts more readily with Syk than the FcγRI/γ-chain complex, contributing to greater phagocytic efficiency of FcγRIIA. Individual Src-related tyrosine kinases (Hck, Lyn) differentially affect phagocytosis and Syk interaction for each receptor. COS-1 cell transfection with FcγRI-γ-γ chimera vs FcγRIIA; co-IP with Syk, Hck, and Lyn; phagocytosis assay with IgG-coated red blood cells Journal of leukocyte biology Medium 15136586
2006 FcγRIA (CD64)-mediated enhancement of dengue virus immune complex infectivity requires signaling competency (intact ITAM) in the accessory γ-chain; abrogation of FcγRIA signaling (by expression without γ-chain or coexpression with ITAM-mutant γ-chain) significantly impairs both phagocytosis and dengue virus immune complex infectivity. This contrasts with FcγRIIA where signaling abrogation impairs phagocytosis but not dengue immune complex infectivity. ITAM tyrosine mutagenesis by site-directed mutagenesis; COS-7 transfection with native and signaling-incompetent FcγRIA/FcγRIIA; dengue virus replication measured by plaque assay and flow cytometry Journal of virology High 17005690
2007 C-reactive protein binds to FcγRI on intact cells with KD ~10 µM; co-expression of the γ-chain markedly increases CRP affinity to FcγRI (~30-fold enhanced association rate, KD ~0.35 µM), suggesting the γ-chain mediates critical transmembrane interactions that enhance CRP binding to FcγRI. Dissociation of CRP from cell surfaces is extremely slow, indicating multivalent binding and receptor clustering. Ultrasensitive confocal imaging analysis (single-molecule); COS-7 transfection with FcγRI alone or FcγRI+γ-chain; binding kinetics measurement The American journal of pathology Medium 17255341
2008 FcγRI (CD64) constitutively resides within lipid raft microdomains (detergent-insoluble buoyant membranes) together with FcR γ-chain, independent of crosslinking ligand. Cholesterol depletion modulates FcγRI-ligand interactions, and FcγRI co-patches with GM1 glycolipid by confocal imaging. Detergent-insoluble membrane fractionation; confocal co-patching with GM1; cholesterol depletion experiments; ligand-binding assay after cholesterol depletion Immunology letters Medium 18207250
2008 Recombinant soluble human FcγRIA (CD64A) binds IgG with high affinity (KD = 1.7×10⁻¹⁰ M), blocks immune complex precipitation, inhibits complement-mediated lysis of antibody-sensitized RBCs, and suppresses immune complex-mediated IL-6, IL-13, MCP-1, and TNF-α production by mast cells. Local or systemic delivery of soluble FcγRIA reduces edema and neutrophil infiltration in the Arthus reaction and prevents joint damage in collagen antibody-induced arthritis in mice. Surface plasmon resonance for binding kinetics; in vitro mast cell cytokine assay; murine Arthus reaction model; collagen antibody-induced arthritis model; 125I-radiolabeling for pharmacokinetics Journal of immunology High 18097060
2009 FcγRI activation triggers a novel signaling cascade linking phospholipase D1 to sphingosine kinase-1 in U937 cells and primary human monocytes, inducing proinflammatory mediator expression and trafficking of immune complexes into HLA-DM-positive antigen-processing compartments with improved MHC class II antigen presentation. This pathway is distinct from FcγRIIA signaling (which uses phospholipase Cγ1 and induces oxidative burst). Pharmacological inhibitor studies (PLD1, SK1); subcellular trafficking analysis with HLA-DM compartment co-localization; cytokine measurement; MHC class II antigen presentation assay; comparison between FcγRI and FcγRIIA activation Blood High 19420354
2010 The FcγRI α-chain (CD64) interacts with OmpA of E. coli K1 independently of IgG opsonization; this interaction requires the full-length α-chain cytoplasmic domain (C-terminal truncation prevents E. coli entry). OmpA binding to FcγRIa prevents γ-chain recruitment and induces a different tyrosine phosphorylation pattern compared with IgG2a-induced phosphorylation. FcγRIa-deficient mice are resistant to E. coli K1 meningitis with accelerated bacterial clearance and increased CR3 expression on macrophages. FcγRIa(-/-) mouse model; overexpression of full-length and C-terminal truncated FcγRIa in COS-1 cells; adoptive macrophage transfer; co-IP to assess γ-chain recruitment; tyrosine phosphorylation immunoblot; CR3 expression flow cytometry PLoS pathogens High 21124939
2010 FcγRI mediates serum amyloid P (SAP)-induced inhibition of fibrocyte differentiation; deletion of FcγRI (CD64) in murine cells or siRNA-mediated knockdown in human cells significantly reduces sensitivity to SAP. The inhibitory receptor FcγRIIb increases sensitivity to SAP, whereas deletion of FcγRIIb, FcγRIIIa, and FcγRIV together does not affect SAP sensitivity. FcγRI-knockout murine cells; siRNA knockdown of FcγRI and FcRγ in human cells; fibrocyte differentiation assay; SAP mutagenesis (residues critical for FcγRIIa binding); genetic deletion combinations Journal of leukocyte biology Medium 22493081
2012 FcγRI (CD64) activation drives NF-κB-regulated NLRP3 inflammasome formation and IL-1β/IL-18 release; FcγRI-expressing Ba/F3 cells show increased NLRP3 inflammasome formation reversed by NF-κB inhibitor PDTC. Silencing FcγRI in THP-1 macrophages reduces NLRP3 inflammasome activation. FcγRI-expressing Ba/F3 cell model; NF-κB inhibitor (PDTC) treatment; siRNA knockdown of FcγRI in THP-1 macrophages; NLRP3 inflammasome protein expression; IL-1β and IL-18 ELISA Life sciences Medium 29920250
2015 Crystal structure of human FcγRI in complex with IgG-Fc reveals the molecular basis for high-affinity binding; a receptor-glycan interaction involving the third extracellular domain contributes importantly to binding affinity. This structural work illuminates how the three-domain architecture of FcγRI achieves high affinity compared to two-domain low-affinity receptors. Structural determination (crystallography of FcγRI–IgG-Fc complex); structural analysis of receptor-glycan contacts Immunological reviews Medium 26497521
2015 Binding of monomeric IgG to FcγRI provides a low-intensity tonic signal necessary for full IFN-γ receptor signaling in the same cell. Engagement of FcγRI with larger immune complexes results in phagocytosis, reactive oxygen species generation, and inflammatory cytokine synthesis, but FcγRI engagement can also potently inhibit IFNγ and TLR4 signaling and induce IL-10 secretion depending on context. Review synthesizing published experimental evidence including receptor signaling studies (tonic signal, IFNγ receptor crosstalk, TLR4 inhibition assays) Immunological reviews Low 26497519
2016 LILRB4 co-ligation with FcγRI significantly dephosphorylates key signaling proteins in the clathrin-mediated endocytosis and Fc-receptor phagocytosis pathways (including FcR γ-chain, Syk, clathrin, Cbl, HRS, TRIM21, and HSP70), suppressing antibody-opsonized bacterial particle uptake, demonstrating that tyrosine phosphorylation of these proteins is critical for FcγRI-dependent endocytosis/phagocytosis. Antibody ligation of FcγRI and/or LILRB4 on THP-1 cells; anti-phosphotyrosine immunoprecipitation; mass spectrometry peptide sequencing (Mascot); Ingenuity Pathway Analysis; bacterial particle phagocytosis assay Scientific reports Medium 27725776
2017 FcγRI (FcγRIa, CD64) nanoclusters at macrophage surfaces are constitutively associated (within 62 ± 5 nm) with SIRPα nanoclusters via the actin cytoskeleton. Upon Fc receptor activation, Src-family kinase signaling causes segregation of FcγRI and SIRPα nanoclusters (to 197 ± 3 nm apart). Co-ligation of SIRPα with CD47 abrogates nanocluster segregation. If activation signals dominate, FcγRI nanoclusters reorganize into periodically spaced concentric rings. Dual-color direct stochastic optical reconstruction microscopy (dSTORM) super-resolution imaging; Src-family kinase inhibitor treatment; CD47-SIRPα co-ligation; actin cytoskeleton disruption The Journal of cell biology High 28289091
2018 Cytokines (IL-3, TNFα, IFNγ) enhance FcγRI binding to immune complexes through 'inside-out' signaling that increases FcγRI nanoclustering in an actin-cytoskeleton-dependent manner. Chemical inhibition of PP1 phosphatase activity reduces FcγRI inside-out signaling (without altering FcγRI phosphorylation itself), and TNFα/IFNγ stimulation enhances neutrophil ADCC toward CD20-expressing tumor cells. Super-resolution imaging (single-particle tracking); PP1 phosphatase inhibitor (calyculin A); actin cytoskeleton disruption; cytokine stimulation (IL-3, TNFα, IFNγ); ADCC assay against CD20+ tumor cells Science signaling High 30042128
2019 FcγRI (CD64) expressed in a subpopulation of joint sensory neurons directly mediates acute joint hypernociception upon IgG immune complex crosslinking, independently of joint inflammation. FcγRI crosslinking directly activates somata and peripheral terminals of these neurons. Effects are diminished in global and sensory-neuron-specific Fcgr1 knockout mice. In murine inflammatory arthritis models, neuronal FcγRI signaling is upregulated and its acute blockade or genetic deletion attenuates arthritis pain without altering joint inflammation. Global and conditional (sensory neuron-specific) Fcgr1 knockout mice; IgG immune complex-induced joint hypernociception model; inflammatory arthritis models; electrophysiology of joint sensory neurons; pain behavioral assays The Journal of clinical investigation High 31211699
2019 Deglycosylation of antibody-based radioimmunoconjugates impairs their binding to FcγRI (surface plasmon resonance, ELISA, flow cytometry), resulting in ~3.5-fold reduction in off-target liver uptake and improved tumor-to-organ contrast in PET imaging in humanized NSG mice, demonstrating that FcγRI-mediated sequestration in immune cells drives hepatic off-target uptake of radioimmunoconjugates. Surface plasmon resonance (SPR); ELISA; flow cytometry; 89Zr-labeling; PET imaging; biodistribution in athymic nude, NSG, and humanized NSG mice bearing HER2+ xenografts Journal of nuclear medicine High 30733320
2021 FcγRI potentiates HIV-1 neutralization by antibodies targeting the gp41 NHR region >5,000-fold in TZM-bl cells expressing FcγRI compared to cells without it, enabling neutralization of tier-2 viruses. This FcγRI-dependent potentiation is also observed with antisera from guinea pigs immunized with an NHR-based vaccine candidate. Neutralization assay in TZM-bl cells with and without FcγRI expression; comparison of tier-1 and tier-2 virus neutralization; guinea pig immunization with (ccIZN36)3 vaccine; FcγRI-blocking controls Proceedings of the National Academy of Sciences of the United States of America Medium 33431684
2022 FCGR1A variants affect CD64 function: (1) SNV rs1848781 in the proximal promoter region associates with CD64 expression levels (confirmed by promoter reporter assay showing higher activity of G vs C allele); (2) rs587598788 indel in intron 5 associates with CD64 expression; (3) non-synonymous SNV rs1050204 (p.D324N) significantly affects CD64-mediated phagocytosis, degranulation, and pro-inflammatory cytokine production. Promoter reporter assay; genotype-phenotype association analysis; functional assays for CD64-mediated phagocytosis, degranulation, and cytokine production with rs1050204 variant Frontiers in immunology Medium 35371020
2023 CD64 overexpression in allogeneic iPSC-derived endothelial cells enables escape from antibody-mediated killing (ADCC and complement-dependent cytotoxicity) by capturing monomeric IgG and occupying Fc regions. An intracellularly truncated CD64 analog (CD64t) retains this protective function, demonstrating that Fc capture rather than intracellular signaling is the mechanistic basis of protection. In vitro ADCC and complement-dependent cytotoxicity assays; humanized mouse ADCC models; overexpression of full-length CD64 vs. intracellularly truncated CD64t; iPSC-derived endothelial cells, thyroid epithelial cells, beta cells, and CAR T cells Nature biotechnology High 36593395
2023 Neuronal FcγRI in dorsal root ganglion (DRG) neurons mediates neuropathic pain; sciatic nerve injury persistently activates FcγRI-related signaling in DRG, and conditional knockout of Fcgr1 in DRG neurons significantly alleviates neuropathic pain. CRP, which increases in DRG after nerve injury, evokes pain by activating neuronal FcγRI. Microinjection of naive IgG into DRG alleviates neuropathic pain by suppressing neuronal FcγRI activation, indicating IgG acts as a competitive inhibitor at neuronal FcγRI. Conditional knockout (CKO) of Fcgr1 in DRG neurons (rat model); nerve injury model (CCI); DRG microinjection of CRP and naive IgG; behavioral pain assays; FcγRI signaling pathway analysis in DRG neurons Advanced science High 36727833
2025 Guselkumab, via its native Fc domain, binds FcγRI (CD64) on IFN-γ-primed monocytes and simultaneously captures IL-23 secreted from CD64+ IL-23-producing macrophages, mediating IL-23 internalization into low-pH intracellular compartments. This Fc-mediated CD64 binding enhances potency for inhibiting IL-23 signaling in a co-culture system where IL-23 is produced by CD64+ cells, compared to risankizumab (which has Fc mutations abrogating FcγR binding). Flow cytometry (Fc-mediated binding to CD64+ monocytes); live-cell confocal imaging (IL-23 internalization into low-pH compartments); co-culture of IL-23-producing CD64+ THP-1 cells with IL-23-responsive reporter cells; Fc-blocking controls Frontiers in immunology Medium 40145093

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 FcgammaRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection. Immunity 223 11911824
2002 FcgammaRI-deficient mice show multiple alterations to inflammatory and immune responses. Immunity 155 11911823
2010 Neutrophil CD64 expression as marker of bacterial infection: a systematic review and meta-analysis. The Journal of infection 133 20206205
2011 Functional characteristics of the high affinity IgG receptor, FcγRI. Journal of immunology (Baltimore, Md. : 1950) 131 21325219
2009 Neutrophil CD64: a diagnostic marker for infection and sepsis. Clinical chemistry and laboratory medicine 128 19642859
2013 The high-affinity human IgG receptor FcγRI (CD64) promotes IgG-mediated inflammation, anaphylaxis, and antitumor immunotherapy. Blood 117 23293080
2012 Neutrophil CD64 expression as a biomarker in the early diagnosis of bacterial infection: a meta-analysis. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases 106 22940278
2017 CD64: An Attractive Immunotherapeutic Target for M1-type Macrophage Mediated Chronic Inflammatory Diseases. Biomedicines 103 28895912
2006 Differential enhancement of dengue virus immune complex infectivity mediated by signaling-competent and signaling-incompetent human Fcgamma RIA (CD64) or FcgammaRIIA (CD32). Journal of virology 103 17005690
2009 Increased expression of FcgammaRI/CD64 on circulating monocytes parallels ongoing inflammation and nephritis in lupus. Arthritis research & therapy 98 19144150
2015 Neutrophil CD64 expression as a diagnostic marker for sepsis in adult patients: a meta-analysis. Critical care (London, England) 92 26059345
1996 Adaptation to eccentric exercise: effect on CD64 and CD11b/CD18 expression. Journal of applied physiology (Bethesda, Md. : 1985) 75 8847330
1999 The FcgammaRIa (CD64) ligand binding chain triggers major histocompatibility complex class II antigen presentation independently of its associated FcR gamma-chain. Blood 72 10397749
2002 C-reactive protein-mediated phagocytosis and phospholipase D signalling through the high-affinity receptor for immunoglobulin G (FcgammaRI). Immunology 66 12383205
2007 Simultaneous quantitative analysis of FcgammaRI (CD64) expression on neutrophils and monocytes: a new, improved way to detect infections. Journal of immunological methods 63 17905303
2007 Neutrophil CD64 (FcgammaRI) expression is a specific marker of bacterial infection: a study on the kinetics and the impact of major surgery. Scandinavian journal of infectious diseases 59 17577814
2000 Therapeutic efficacy of FcgammaRI/CD64-directed bispecific antibodies in B-cell lymphoma. Blood 59 11071653
1994 The high affinity Fc gamma receptor (CD64) induces phagocytosis in the absence of its cytoplasmic domain: the gamma subunit of Fc gamma RIIIA imparts phagocytic function to Fc gamma RI. Experimental hematology 59 7516890
2022 CD66b-CD64dimCD115- cells in the human bone marrow represent neutrophil-committed progenitors. Nature immunology 55 35484408
2019 The Impact of FcγRI Binding on Immuno-PET. Journal of nuclear medicine : official publication, Society of Nuclear Medicine 55 30733320
2011 Neutrophil CD64 as a sepsis biomarker. Biochemia medica 55 22420242
2007 Hematological indices, inflammatory markers and neutrophil CD64 expression: comparative trends during experimental human endotoxemia. Journal of endotoxin research 53 17621550
1998 The second and third extracellular domains of FcgammaRI (CD64) confer the unique high affinity binding of IgG2a. Molecular immunology 52 9881694
2020 The Influence of Glycans-Specific Bioconjugation on the FcγRI Binding and In vivo Performance of 89Zr-DFO-Pertuzumab. Theranostics 51 32042334
2019 Neuronal FcγRI mediates acute and chronic joint pain. The Journal of clinical investigation 51 31211699
2009 Differential signal transduction, membrane trafficking, and immune effector functions mediated by FcgammaRI versus FcgammaRIIa. Blood 50 19420354
2017 Membrane nanoclusters of FcγRI segregate from inhibitory SIRPα upon activation of human macrophages. The Journal of cell biology 48 28289091
2015 The many faces of FcγRI: implications for therapeutic antibody function. Immunological reviews 48 26497519
2010 The novel applications of the quantitative analysis of neutrophil cell surface FcgammaRI (CD64) to the diagnosis of infectious and inflammatory diseases. Current opinion in infectious diseases 45 20407370
2012 FcγRI mediates serum amyloid P inhibition of fibrocyte differentiation. Journal of leukocyte biology 44 22493081
2024 An engineered α1β1 integrin-mediated FcγRI signaling component to control enhanced CAR macrophage activation and phagocytosis. Journal of controlled release : official journal of the Controlled Release Society 42 39617174
2013 CD64-Neutrophil expression and stress metabolic patterns in early sepsis and severe traumatic brain injury in children. BMC pediatrics 42 23452299
2018 Immunophenotyping of Monocytes During Human Sepsis Shows Impairment in Antigen Presentation: A Shift Toward Nonclassical Differentiation and Upregulation of FCγRi-Receptor. Shock (Augusta, Ga.) 41 29668526
2012 Fc gamma receptor CD64 modulates the inhibitory activity of infliximab. PloS one 41 22937039
2004 Direct interaction between FcgammaRI (CD64) and periplakin controls receptor endocytosis and ligand binding capacity. Proceedings of the National Academy of Sciences of the United States of America 41 15229321
2001 Enhancement of polymorphonuclear cell-mediated tumor cell killing on simultaneous engagement of fcgammaRI (CD64) and fcalphaRI (CD89). Cancer research 40 11358825
2008 Destructive arthritis in the absence of both FcgammaRI and FcgammaRIII. Journal of immunology (Baltimore, Md. : 1950) 39 18354234
2023 Protection of cell therapeutics from antibody-mediated killing by CD64 overexpression. Nature biotechnology 37 36593395
2015 Structural mechanism of high affinity FcγRI recognition of immunoglobulin G. Immunological reviews 36 26497521
2010 Fcγ receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1. PLoS pathogens 36 21124939
2000 Production of macrophage-activated killer cells for targeting of glioblastoma cells with bispecific antibody to FcgammaRI and the epidermal growth factor receptor. Cancer immunology, immunotherapy : CII 36 11092616
2018 FcγRI (CD64) contributes to the severity of immune inflammation through regulating NF-κB/NLRP3 inflammasome pathway. Life sciences 34 29920250
2005 Neutrophil CD64 expression in Behçet's disease. The Journal of rheumatology 34 15868620
2004 FcgammaRIIa expression with FcgammaRI results in C-reactive protein- and IgG-mediated phagocytosis. Journal of leukocyte biology 32 15075346
2018 Mechanisms of inside-out signaling of the high-affinity IgG receptor FcγRI. Science signaling 31 30042128
2017 Neutrophil CD64, C-reactive protein, and procalcitonin in the identification of sepsis in the ICU - Post-test probabilities. Journal of critical care 31 28898742
2010 Targeting allergen to FcgammaRI reveals a novel T(H)2 regulatory pathway linked to thymic stromal lymphopoietin receptor. The Journal of allergy and clinical immunology 31 20109752
2020 Effect of neutrophil CD64 for diagnosing sepsis in emergency department. World journal of emergency medicine 30 32076472
2018 Combined CD25, CD64, and CD69 biomarker panel for flow cytometry diagnosis of sepsis. Talanta 29 30262053
2008 FcgammaRI (CD64) resides constitutively in lipid rafts. Immunology letters 29 18207250
2016 Neutrophil CD64 expression as a longitudinal biomarker for severe disease and acute infection in critically ill patients. International journal of laboratory hematology 28 27565453
1999 Differentiation-dependent switch in protein kinase C isoenzyme activation by FcgammaRI, the human high-affinity receptor for immunoglobulin G. Immunology 28 10233728
2016 Meta-analysis of diagnostic accuracy of neutrophil CD64 for neonatal sepsis. Italian journal of pediatrics 27 27268050
2019 Smartphone-imaged microfluidic biochip for measuring CD64 expression from whole blood. The Analyst 26 31094395
2010 Identification of IgG(1) variants with increased affinity to FcγRIIIa and unaltered affinity to FcγRI and FcRn: comparison of soluble receptor-based and cell-based binding assays. Journal of immunological methods 26 21185301
2009 Recombinant soluble human FcgammaR1A (CD64A) reduces inflammation in murine collagen-induced arthritis. Journal of immunology (Baltimore, Md. : 1950) 26 19454724
2008 Targeting immune complex-mediated hypersensitivity with recombinant soluble human FcgammaRIA (CD64A). Journal of immunology (Baltimore, Md. : 1950) 26 18097060
2005 CD64 (Fcgamma receptor I) cell surface expression on maturing neutrophils from preterm and term newborn infants. Acta paediatrica (Oslo, Norway : 1992) 26 16028647
2004 Depletion of synovial macrophages in rheumatoid arthritis by an anti-FcgammaRI-calicheamicin immunoconjugate. Annals of the rheumatic diseases 26 15539412
1999 The cytoplasmic domain of human FcgammaRIa alters the functional properties of the FcgammaRI.gamma-chain receptor complex. The Journal of biological chemistry 26 10514529
2025 Guselkumab binding to CD64+ IL-23-producing myeloid cells enhances potency for neutralizing IL-23 signaling. Frontiers in immunology 25 40145093
2022 Targeting the high affinity receptor, FcγRI, in autoimmune disease, neuropathy, and cancer. Immunotherapy advances 25 36284837
2016 Leukocyte immunoglobulin-like receptor B4 regulates key signalling molecules involved in FcγRI-mediated clathrin-dependent endocytosis and phagocytosis. Scientific reports 25 27725776
2018 Lentivirus-mediated knockdown of FcγRI (CD64) attenuated lupus nephritis via inhibition of NF-κB regulating NLRP3 inflammasome activation in MRL/lpr mice. Journal of pharmacological sciences 23 30190171
2016 Expression of CD64 on Circulating Neutrophils Favoring Systemic Inflammatory Status in Erythema Nodosum Leprosum. PLoS neglected tropical diseases 23 27556927
2015 Kinetics of leukocyte CD11b and CD64 expression in severe sepsis and non-infectious critical care patients. Acta anaesthesiologica Scandinavica 23 25866876
2004 Modulation of FcgammaRI (CD64) ligand binding by blocking peptides of periplakin. The Journal of biological chemistry 23 15161926
1999 Role of FcgammaRI (CD64) in erythrocyte elimination and its up-regulation in thalassaemia. British journal of haematology 23 10519993
1997 Humanized mAb H22 binds the human high affinity Fc receptor for IgG (FcgammaRI), blocks phagocytosis, and modulates receptor expression. Journal of leukocyte biology 23 9335317
2021 The high-affinity immunoglobulin receptor FcγRI potentiates HIV-1 neutralization via antibodies against the gp41 N-heptad repeat. Proceedings of the National Academy of Sciences of the United States of America 21 33431684
2021 High expression of neutrophil and monocyte CD64 with simultaneous lack of upregulation of adhesion receptors CD11b, CD162, CD15, CD65 on neutrophils in severe COVID-19. Therapeutic advances in infectious disease 21 34377464
2013 Are neutrophil CD64 expression and interleukin-6 early useful markers for diagnosis of acute appendicitis? European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift fur Kinderchirurgie 21 23757034
2005 Cell surface expression of FcgammaRI (CD64) on neutrophils and monocytes in patients with influenza A, with and without complications. Scandinavian journal of infectious diseases 21 16308225
2023 Neuronal C-Reactive Protein/FcγRI Positive Feedback Proinflammatory Signaling Contributes to Nerve Injury Induced Neuropathic Pain. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20 36727833
2019 Diagnostic value of neutrophil CD64 combined with CRP for neonatal sepsis: A meta-analysis. The American journal of emergency medicine 20 31085013
2018 Neutrophil CD64, TLR2 and TLR4 expression increases but phagocytic potential decreases during tuberculosis. Tuberculosis (Edinburgh, Scotland) 20 30029898
2007 Affinity of C-reactive protein toward FcgammaRI is strongly enhanced by the gamma-chain. The American journal of pathology 20 17255341
2007 Hyperexpression of FcgammaRI and Toll-like receptor 4 in the intestinal mast cells of Crohn's disease patients. Clinical immunology (Orlando, Fla.) 20 17827066
2006 Molecular cloning and expression of the porcine high-affinity immunoglobulin G Fc receptor (FcgammaRI). Immunogenetics 20 16912901
2002 The CY domain of the Fcgamma RIa alpha-chain (CD64) alters gamma-chain tyrosine-based signaling and phagocytosis. The Journal of biological chemistry 20 12200451
2013 Diagnostic accuracy of neutrophil CD64 expression in neonatal infection: a meta-analysis. The Journal of international medical research 19 23867450
2010 Brucella abortus inhibits IFN-γ-induced FcγRI expression and FcγRI-restricted phagocytosis via toll-like receptor 2 on human monocytes/macrophages. Microbes and infection 19 21070860
2018 Neutrophil CD64 expression, procalcitonin and presepsin are useful to differentiate infections from flares in SLE patients with SIRS. Lupus 18 29540108
2018 The alternatively spliced porcine FcγRI regulated PRRSV-ADE infection and proinflammatory cytokine production. Developmental and comparative immunology 18 30273630
1999 Influence of the human high-affinity IgG receptor FcgammaRI (CD64) on residual infectivity of neutralized dengue virus. Virology 18 10405359
2024 Crosstalk between CD64+MHCII+ macrophages and CD4+ T cells drives joint pathology during chikungunya. EMBO molecular medicine 17 38332201
2023 Development of an Aptamer-Based Molecular Tool for Specifically Targeting Microglia via the CD64 Protein. Analytical chemistry 16 36716100
2022 Examination of IgG Fc Receptor CD16A and CD64 Expression by Canine Leukocytes and Their ADCC Activity in Engineered NK Cells. Frontiers in immunology 16 35281028
2022 Novel Human FCGR1A Variants Affect CD64 Functions and Are Risk Factors for Sarcoidosis. Frontiers in immunology 16 35371020
2021 Evaluating the Timeliness and Specificity of CD69, CD64, and CD25 as Biomarkers of Sepsis in Mice. Shock (Augusta, Ga.) 16 32890312
2008 Expression of CD64, CD206, and RAGE in adherent cells of diabetic patients infected with Mycobacterium tuberculosis. Archives of medical research 16 18279703
2001 Tumor cells express FcgammaRI which contributes to tumor cell growth and a metastatic phenotype. Neoplasia (New York, N.Y.) 16 11420747
2000 Mouse FcgammaRI: identification and functional characterization of five new alleles. Immunogenetics 16 10752630
2018 Fc gamma receptor binding profile of anti-citrullinated protein antibodies in immune complexes suggests a role for FcγRI in the pathogenesis of synovial inflammation. Clinical and experimental rheumatology 15 29352854
2015 The high-affinity receptor for IgG, FcγRI, of humans and non-human primates. Immunological reviews 15 26497520
2009 Fcgamma receptor 1 (CD64), a target beyond cancer. Current pharmaceutical design 15 19689341
2004 The monocyte Fcgamma receptors FcgammaRI/gamma and FcgammaRIIA differ in their interaction with Syk and with Src-related tyrosine kinases. Journal of leukocyte biology 15 15136586
2024 CD64+ fibroblast-targeted vilanterol and a STING agonist augment CLDN18.2 BiTEs efficacy against pancreatic cancer by reducing desmoplasia and enriching stem-like CD8+ T cells. Gut 14 39187291
1998 FcgammaRIa-gamma-chain complexes trigger antibody-dependent cell-mediated cytotoxicity (ADCC) in CD5+ B cell/macrophage IIA1.6 cells. Clinical and experimental immunology 14 9737671
1996 Extracellular mutations of non-obese diabetic mouse FcgammaRI modify surface expression and ligand binding. The Journal of biological chemistry 14 8663283

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