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FcalphaRI-induced cytokine production is orchestrated via upregulation of cytokine translation and caspase-1 activation, which is dependent on glycolytic reprogramming.
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In transgenic mice, IgAN pathogenesis involves impaired clearance of abnormal IgA via CD89, primarily by the Kupffer cells. Conditional IgAN progression in CD89 transgenic mice thus reveals important aspects of IgAN pathogenesis.
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a novel Fcar splice variant termed variant APD isolated from a healthy volunteer that lacks only the IgA-binding EC1 domain, is reported.
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Findings suggest a basis for the use of Fc receptor I for IgA (FcalphaRI) as a molecular target for the treatment of lupus.
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induces different forms of neutrophil death, depending on the inflammatory microenvironment
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this study examined the expression of IL-4 mRNA, IFN-c mRNA and FcaRI mRNA in tonsillar mononuclear cells of IgA nephropathy9(IgAN) patients and non-IgAN patients.
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FCAR polymorphism is not associated with high susceptibility to IGA nephropathy in caucasians.
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Abnormally glycosylated IgA1 and soluble CD89-IgA and IgA-IgG complexes, features of primary IgA nephropathy, are also present in alcoholic cirrhosis.
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Genetic variation at the promoter region of IgA receptor is associated with IgA nephropathy.
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These results suggest a role of anti-FcaRI Fab as a negative regulator in controlling the magnitude of the innate immune response
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Glycosylation of the CH2/CH3 interface inhibits interaction with the pathogen IgA binding protein SSL7, while maintaining binding of pIgR, essential to the biosynthesis and transport of SIgA.
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In this study, human mammary carcinoma cells are efficiently killed when incubated with human neutrophils and tumor-specific FcalphaRI bispecific or immunoglobulin A antibodies.
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Data show that the Fc(alpha)RI 844 A>G polymorphism is not associated with systemic sclerosis or rheumatoid arthritis sceptibility.
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FcalphaRI defines a function for pentraxins in inflammatory responses involving neutrophils and macrophages. It also highlights the innate aspect of otherwise humoral immunity-associated antibody receptors.
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There is an association between the levels of sCD89-IgA complexes in serum and the severity of IgA nephropathy, and a possible genetic component in regulating the production or expression of sCD89.
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Endocytosis of FcalphaR is clathrin- and dynamin-dependent, but is not regulated by Rab5, and the endocytic motif is not located in the cytoplasmic domain of FcalphaR.
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CD89 circulates in a high molecular mass form in complex covalently linked to IgA and contributes to the formation of polymeric serum IgA.
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study suggests that expression of the FcR splice isoform DeltaEC2 but not Delta66EC2 is differentially regulated in a cell type-specific manner and in response to inflammatory and/or infectious processes
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The Fc alpha receptor 5'-flanking region from -102 to -64 relative to the ATG translation initiation codon is essential for promoter activity and contains two functional binding motifs for C/EBP and Ets family members at -74 and -92, respectively.
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there is a bivalent, pH-dependent interaction between FcalphaRI and IgA with important implications for cytokine-dependent phagocytosis of IgA and the FcalphaRI-mediated degradation or recycling of IgA
