Disease relevance of FCGR1B

• Differential Enhancement of Dengue Virus Immune Complex Infectivity Mediated by Signaling-Competent and Signaling-Incompetent Human Fc{gamma}RIA (CD64) or Fc{gamma}RIIA (CD32) [1].
• In vivo targeting of human neuroblastoma xenograft by anti-GD2/anti-Fc gamma RI (CD64) bispecific antibody [2].
• In the present report we review the literature suggesting that CD64-targeted antigens are likely to be effective in vivo, and present data demonstrating enhanced immunogenicity in CD64 transgenic mice of a fusion protein that combines the specificities of HIV gp120 and the humanized anti-CD64 monoclonal antibody H22 [3].
• The class I IgG receptor (Fc gamma RI or CD64 receptor), which is present on key cytotoxic effector cells, has been shown to initiate the destruction of tumor cells in vitro and has been hypothesized to play a role in the destruction of antibody-coated cells such as platelets in idiopathic thrombocytopenia purpura (ITP) [4].
• CD64 expression on neutrophils might therefore be a potential candidate for the diagnosis of bacterial infections in infants [5].

High impact information on FCGR1B

• Impaired response to IFN-gamma was documented in B cells by signal transducer and activator of transcription 1 nuclear translocation, in fibroblasts by cell surface HLA class II induction, and in monocytes by cell surface CD64 induction and TNF-alpha secretion [6].
• In this study, we demonstrate enhanced presentation of antigenic and antagonistic peptides by targeting them to the type I Fc receptor for IgG (F(c)gammaRI, CD64) on human monocytes [7].
• These CD64-targeted peptides were up to 1,000- and 100-fold more efficient than the parent peptides for T cell stimulation and antagonism, respectively, suggesting that such fusion proteins could effectively increase the delivery of peptides to APCs in vivo [7].
• Evaluations were made on oxidative capacity, measured by superoxide anion production and chemiluminescence after stimulation with f-met-leu-phe (f-MLP) or phorbol-myristate-acetate, the killing of Aspergillus fumigatus hyphae (assessed as conversion of the tetrazolium salt MTT to formazan), and on the expression of Fc gammaRI receptor (CD64) [8].
• Granulocyte colony-stimulating factor induces hFc gamma RI (CD64 antigen)-positive neutrophils via an effect on myeloid precursor cells [9].

Chemical compound and disease context of FCGR1B

• K1m also expresses Fc receptors for immunoglobulin G (IgG) (CD64, CD32, and CD16) and can be shown to phagocytose polystyrene latex beads, as well as neuroblastoma cells in the presence of tumour-specific monoclonal antibody (mAb) [10].
• The neutropenia induced by the thalidomide analogue CC-4047 in patients with multiple myeloma is associated with an increased percentage of neutrophils bearing CD64 [11].

Biological context of FCGR1B

• Curiously, the three genes in this recently duplicated gene family flank the centromere of human chromosome 1, with FCGR1B located at 1p12 and both FCGR1A and FCGR1C located at 1q21 [12].
• We studied the activation of the human PMN oxidative burst and stimulated fluid pinocytosis induced by three monoclonal antibodies (MoAbs) directed against Fc gamma RI (CD64) to study the role of this receptor in Fc-mediated cellular activation [13].
• By blocking CD16 and CD64 molecules with anti-CD16 and anti-CD64 MAb, a significant down-regulation of MAb18B7-induced fungicidal activity was observed [14].
• BsAbs directed to either FcgammaRI (CD64) or FcalphaRI (CD89) on human PMNL effectively enhanced both phagocytosis and killing of C. albicans in vitro [15].
• Neutrophil phenotype changes after rhG-CSF administration: immediate effects cause direct activation of circulating neutrophils, but delayed effects are characterized by increased surface expression of important effector molecules directly involved in neutrophil functions, such as CD14, CD32, CD64 [16].

Anatomical context of FCGR1B

• Inflammatory macrophages have increased expression of CD64, the high-affinity receptor for IgG [17].
• T cell proliferation experiments performed with the use of Fc gamma R-transfected fibroblasts as accessory cells showed the high affinity Fc gamma RIa (CD64) to interact with both rat IgG2b and rat IgG2b-mlgG1 hybrid CD3 mAb [18].
• In this study, we show elevated levels of CD64 on synovial macrophages in both synovial lining and synovial fluid in RA patients [17].
• The expression of the high-affinity receptor for IgG, CD64, on monocytes was significantly enhanced after IVIg infusion, while the low-affinity receptor for IgG, CD32, was only slightly increased [19].
• Enhanced expression of HLA-DR, Fc gamma receptor 1 (CD64) and leukocyte common antigen (CD45) indicate activation of monocytes in regenerative training periods of endurance athletes [20].

Associations of FCGR1B with chemical compounds

• Monomeric immunoglobulin G was used as a specific ligand for CD64 followed by measurements of superoxide anion, hypochlorous acid, and N-acetyl-beta-glucosaminidase production to measure oxidative metabolism and azurophilic granule degranulation [21].
• We found that the expression of the membrane antigens CD64, CD66, and CD67 by granulocytes was inversely associated with the luminal renarrowing normalized for vessel size (relative loss) at 6 months after PTCA, while the production of IL-1 beta by stimulated monocytes was positively associated with the relative loss [22].
• We found that the entire HUS AP Mo population exhibited reduced CD14, CD64, and CD11b expression and decreased LPS-induced tumor necrosis factor production and Fcgamma-dependent cytotoxicity [23].
• In vitro monocyte HLA-DR and FcgammaRI/CD64 expression is dependent on glutamine availability [24].
• Patients with active disease had increased monocyte activation compared with healthy controls as shown by increased concentrations of neopterin (p < 0.0001) and increased surface expression of CD11b (p < 0.05) and CD64 (p < 0.05) [25].

Analytical, diagnostic and therapeutic context of FCGR1B

• To examine whether killing of CD64 macrophages results in therapeutic effects in vivo, we established an adjuvant arthritis (AA) model in newly generated human CD64 (hCD64) transgenic rats [17].
• Clinical experience with CD64-directed immunotherapy. An overview [4].
• METHODS: Cell surface expression of CD64 on neutrophils from preterm and term newborn infants and healthy adults was analysed by flow cytometry [5].
• As an approach to understanding their role in neonatal life, we have compared the constitutive expression of the three Fc receptors--Fc gamma RI (CD64), Fc gamma RII (CD32) and Fc gamma RIII (CD16)--by neonatal and adult blood monocytes and granulocytes using quantitative immunofluorescence by flow cytometry [26].
• Human high-affinity Fc gamma RI (CD64) gene mapped to chromosome 1q21.2-q21.3 by fluorescence in situ hybridization [27].

References