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Collectively, these results indicate that the amino acid substitution Ala78Asp resulting in the HNA-1c allotype leads to higher affinity toward human IgG, enhancement of neutrophil activation, and possibly effective clearance of malaria by intracellular reactive oxygen species.
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SHP-2 is activated by CD16b crosslinking in neutrophils.
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FCGR3B deficiency due to copy number variations may predispose to eosinophilic granulomatosis with polyangiitis.
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low copy numbers of FCGR2A and FCGR3B to be common risk factors for systemic lupus nephritis (SLE) and ANCA-associated systemic vasculitis (AASV).
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The FCGR3B NA1/NA1 genotype is associated with hypersensitivity reactions to adalimumab in Japanese patients with Rheumatoid Arthritis.
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Data suggest association of FCGR3B deletion with increased risk of rheumatoid arthritis (RA) in a large cohort.
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Gene copy number variation (CNV) of the PKLR, FCGR2A, FCGR2C, and FCGR3 genes is associated with malaria severity, and our results provide evidence for a role of CNV in host responses to malaria.
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Association between Fc gamma Receptor IIIB genetic polymorphisms and susceptibility to severe malaria anemia in children in western Kenya.
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We conclude that FCGR3A CNVs are a major risk factor for female sarcoidosis and FCGR3B CNVs may also affect the development of sarcoidosis.
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CD16 and CD35 are important for neutrophil internalization of M. tuberculosis, whereas HIV-1 infection adversely affects opsonophagocytosis.
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There was no aberration in FCGR3B allele/genotype frequencies in sarcoidosis patients compared to controls.
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Results showed that susceptibility to systemic lupus erythematosus was associated with the FCGR3B*01 allele, as well as with the FCGR3B*01/*01 and FCGR3B*01/*02 genotypes.
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FcgammaRIIIB allelic distribution was similar among pediatric Guillain-Barre syndrome patients and controls.
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Lower copy numbers (
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This metaanalysis indicates that polymorphisms in the pathways of immune complex clearance, such as the FcgammaRIIIa, FcgammaRIIIb, and ITGAM genotypes, are potential susceptibility genes for neuropsychiatric systemic lupus erythematosus.
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data show that cross-linking FcgammaRIIIb is responsible for NET formation by the human neutrophil
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our method allows determining the CNV status of the FCGR locus, we identified association of CNV in FCGR3B to RA and showed a functional relationship between CNV in the FCGR3A gene and CD16A expression.
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Fc-gamma receptor polymorphisms differentially influence susceptibility to systemic lupus erythematosus and lupus nephritis.
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the results of this meta-analysis indicated that low FCGR3B CN increased susceptibility to autoimmune diseases--{REVIEW}
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Data show that gains or losses in copy numbers of Fc gamma receptors FCGR3A were less frequent than for FCGR3B and FCGR2C.
