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Gwan Gyu Song - One of the best experts on this subject based on the ideXlab platform.
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associations between functional FCGR2A r131h and fcgr3a f158v polymorphisms and responsiveness to tnf blockers in spondyloarthropathy psoriasis and crohn s disease a meta analysis
Pharmacogenomics, 2016Co-Authors: Young Ho Lee, Sung Jae Choi, Gwan Gyu SongAbstract:Aim: The aim of the current study was to investigate whether FCGR polymorphisms are associated with responsiveness to anti-TNF-α therapy in patients with spondyloarthropathy, psoriasis, and Crohn's disease. Materials & methods: We conducted a meta-analysis to evaluate the association between the functional FCGR3A F158V and FCGR2A R131H polymorphisms and responsiveness to TNF blockers. Results: The meta-analysis indicated that responsiveness to TNF blockers was associated with the FCGR3A V allele (odds ratio: 3.308; 95% CI: 1.053–10.39; p = 0.040) and the FCGR2A RR + RH genotype (odds ratio: 3.904; p = 0.027) in patients with a follow-up time of ≥6 months. Conclusion: FCGR3A V and FCGR2A R allele carriers show better responsiveness to anti-TNF-α therapy in patients with follow-up times ≥6 months.
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FCGR2A fcgr3a fcgr3b polymorphisms and susceptibility to rheumatoid arthritis a meta analysis
Clinical and Experimental Rheumatology, 2015Co-Authors: Gwan Gyu SongAbstract:Abstract The aim of this study is to explore whether Fc gamma receptor (FCGR) polymorphisms are associated with the susceptibility to rheumatoid arthritis (RA). We conducted a meta-analysis on the association between FCGR2A H131R (rs1801274), FCGR3A F158V (rs396991), and FCGR3B NA1/NA2 polymorphisms and RA susceptibility. A total of seventeen studies reported in fourteen articles (4,418 patients with RA and 3,560 controls) were considered in our meta-analysis. In all of the study subjects, meta-analysis indicated an association between RA and FCGR2A R allele (OR=0.877, 95% CI=0.792-0.971, p=0.011). Stratification by ethnicity indicated an association between FCGR2A R allele and RA in Europeans (OR=0.816, 95% CI=0.687-0.968, p=0.020), but not in East Asians (OR=0.900, 95% CI=0.778-1.040, p=0.154). Meta-analysis revealed an association between RA and FCGR3A VV vs. FF genotype in all the study subjects (OR=1.210, 95% CI=1.067-1.479, p=0.006). Stratification by ethnicity indicated an association between FCGR3A VV genotype and RA compared toFF genotype in Europeans (OR=1.350, 95% CI=1.107-1.646, p=0.003), but not in East Asians and South Asians. No association was observed between RA and FCGR3B polymorphisms on performing the meta-analysis. Although no relationship was found between the FCGR3B polymorphism and RA susceptibility, FCGR2A and FCGR3A polymorphisms were found to be associated with RA in Europeans, but not in Asians.
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FCGR2A fcgr3a fcgr3b polymorphisms and susceptibility to rheumatoid arthritis a meta analysis
Clinical and Experimental Rheumatology, 2015Co-Authors: Young Ho Lee, Sang Cheol Bae, Gwan Gyu SongAbstract:OBJECTIVES The aim of this study is to explore whether Fc gamma receptor (FCGR) polymorphisms are associated with the susceptibility to rheumatoid arthritis (RA). METHODS We conducted a meta-analysis on the association between FCGR2A H131R (rs1801274), FCGR3A F158V (rs396991), and FCGR3B NA1/NA2 polymorphisms and RA susceptibility. RESULTS A total of seventeen studies reported in fourteen articles (4,418 patients with RA and 3,560 controls) were considered in our meta-analysis. In all of the study subjects, meta-analysis indicated an association between RA and FCGR2A R allele (OR=0.877, 95% CI=0.792-0.971, p=0.011). Stratification by ethnicity indicated an association between FCGR2A R allele and RA in Europeans (OR=0.816, 95% CI=0.687-0.968, p=0.020), but not in East Asians (OR=0.900, 95% CI=0.778-1.040, p=0.154). Meta-analysis revealed an association between RA and FCGR3A VV vs. FF genotype in all the study subjects (OR=1.210, 95% CI=1.067-1.479, p=0.006). Stratification by ethnicity indicated an association between FCGR3A VV genotype and RA compared toFF genotype in Europeans (OR=1.350, 95% CI=1.107-1.646, p=0.003), but not in East Asians and South Asians. No association was observed between RA and FCGR3B polymorphisms on performing the meta-analysis. CONCLUSIONS Although no relationship was found between the FCGR3B polymorphism and RA susceptibility, FCGR2A and FCGR3A polymorphisms were found to be associated with RA in Europeans, but not in Asians.
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associations between FCGR2A rs1801274 fcgr3a rs396991 fcgr3b na1 na2 polymorphisms and periodontitis a meta analysis
Molecular Biology Reports, 2013Co-Authors: Gwan Gyu SongAbstract:The aim of this study was to determine whether the Fcγ receptors (FCGRs) polymorphisms confer susceptibility to periodontitis in ethnically different populations. We did a literature search using PubMed and Embase, and conducted a meta-analysis on the associations between the FCGR2A H131R (rs1801274), FCGR3A F158V (rs396991), and FCGR3B NA1/NA2 polymorphisms and periodontitis using allele contrast, the recessive model, the dominant model, and the homozygote contrast. A total of 17 separate comparisons with 1,421 patients with periodontitis and 1,454 controls, involving six Caucasian, six East Asian, two African and one South Asian population were considered in the meta-analysis. Meta-analysis of the FCGR2A H131R polymorphism showed no association between periodontitis and the FCGR2A R allele (OR = 0.987, 95 % CI = 0.881–1.107, p = 0.827). Stratification by ethnicity revealed an association between the RR+RH genotype with periodontitis in Caucasian population (OR = 0.624, 95 % CI = 0.479–0.813, p = 4.7 × 10−5), but not in East Asian, and African populations. Meta-analysis of the FCGR3A F158V polymorphism revealed an association between the FCGR3A V allele and periodontitis is in Caucasians (OR = 1.457, 95 % CI = 1.014–2.092, p = 0.042), but not in East Asians and Africans. In addition, analysis using the dominant model and homozygote contrast showed the same pattern for the FCGR3A V allele. Meta-analysis of the FCGR3B NA1/NA2 polymorphism using the recessive model revealed a significant association between the NA2/NA2 genotype and periodontitis in aggressive periodontitis (OR = 2.853, 95 % CI = 1.673–4.863, 1.1 × 10−5). This meta-analysis demonstrates that the FCGR2A, and FCGR3A polymorphisms may confer susceptibility to periodontitis in Caucasians, and that the FCGR3B polymorphism may be associated with susceptibility to aggressive periodontitis.
Alexander Dobrovic - One of the best experts on this subject based on the ideXlab platform.
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a critical review of the role of fc gamma receptor polymorphisms in the response to monoclonal antibodies in cancer
Journal of Hematology & Oncology, 2013Co-Authors: James D Mellor, Michael P Brown, Helen Irving, John Zalcberg, Alexander DobrovicAbstract:Antibody-dependent cellular cytotoxicity (ADCC) is a major mechanism of action of therapeutic monoclonal antibodies (mAbs) such as cetuximab, rituximab and trastuzumab. Fc gamma receptors (FcgR) on human white blood cells are an integral part of the ADCC pathway. Differential response to therapeutic mAbs has been reported to correlate with specific polymorphisms in two of these genes: FCGR2A (H131R) and FCGR3A (V158F). These polymorphisms are associated with differential affinity of the receptors for mAbs. This review critically examines the current evidence for genotyping the corresponding single nucleotide polymorphisms (SNPs) to predict response to mAbs in patients with cancer.
Jicheng Lv - One of the best experts on this subject based on the ideXlab platform.
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low copy numbers of fcgr3a and fcgr3b associated with chinese patients with sle and aasv
Lupus, 2017Co-Authors: Y Qi, D Bu, Jicheng LvAbstract:Low-affinity Fcγ receptors (FcγR) act as key mediators of the pathogenic effects of autoantibodies. In this study, we aimed to determine whether copy number variations (CNVs) in FCGR3A and FCGR3B were associated with systemic lupus nephritis (SLE) and ANCA-associated systemic vasculitis (AASV) in Chinese individuals. A total of 1118 individuals were enrolled, including 415 SLE patients, 139 AASV patients, and 564 healthy controls. FCGR3A and FCGR3B copy numbers (CNs) were determined by both a paralogue ratio test and TaqMan quantitative PCR assay. In the susceptibility associations, a low FCGR3B CN was significantly associated with SLE ( p = 5.01 × 10-3; odds ratio (OR) 1.71; 95% confidence interval (CI) 1.17-2.48) and AASV ( p = 0.04; OR = 1.72; 95% CI 1.02-2.88). A low FCGR3A CN was also significantly associated with SLE ( p = 6.02 × 10-3; OR 2.72; 95% CI 1.30-5.71) and AASV ( p = 0.042; OR 2.64; 95% CI 1.00-6.93). Further subphenotype analysis revealed that low CNs of FCGR3A and FCGR3B were significantly associated with clinical manifestations in SLE and AASV patients. Therefore, in this case-control study, we identified low CNs of FCGR2A and FCGR3B to be common risk factors for SLE and AASV.
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copy number variation of fcgr3a rather than fcgr3b and fcgr2b is associated with susceptibility to anti gbm disease
International Immunology, 2010Co-Authors: Xujie Zhou, Yanrong Yang, Jicheng Lv, Dingfang Bu, Minghui Zhao, Lei Yu, Juan Zhao, Rui Yang, Hong ZhangAbstract:Anti-glomerular basement membrane antibody disease (anti-GBM disease) is a rare disorder characteristic of universally poor outcome. Fcg receptors (FcgRs) play important roles in anti-GBM disease based on evidence from animal models. Copy number variation (CNV) influences disease susceptibility. The FcgRs genes show CNV, and CNV of the FCGR3B gene is associated with glomerulonephritis in systemic lupus erythematosus and anti-neutrophil cytoplasmic antibodyassociated small vasculitis. Here, we investigated CNV of three FCGR genes, including two (FCGR3A and FCGR3B) for activating FcgRs and one (FCGR2B) for inhibitory FcgR by duplex quantitative realtime PCR. Copy numbers were analyzed by Applied Biosystems CopyCaller Software v1.0. We first demonstrated the distribution of CNV of FCGR3A, FCGR3B and no CNV of FCGR2B in Chinese population (including 47 anti-GBM patients and 146 healthy controls). The frequency of CNV of FCGR3A was observed to be significantly higher than matched healthy controls (27.7 versus 12.3%, P 5 0.013, odds ratio 1.21‐6.10). Considering previous report about gene knock-out animal models and CNV effect of FCGR3A, we thus propose that CNV in members of FCGR family should have different roles in the pathogenesis of human anti-GBM disease.
Michiaki Kubo - One of the best experts on this subject based on the ideXlab platform.
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impact of allele copy number of polymorphisms in fcgr3a and fcgr3b genes on susceptibility to ulcerative colitis
Inflammatory Bowel Diseases, 2013Co-Authors: Kouichi Asano, Junji Umeno, Naoya Hosono, Yutaka Kiyohara, Atsushi Hirano, Motohiro Esaki, Takayuki Matsumoto, Toshiyuki Matsui, Michiaki KuboAbstract:Abstract Polymorphisms in the Fcγ receptor genes have been implicated in several autoimmune diseases, including ulcerative colitis (UC). However, most of these reports had not taken into account the effect of copy number variation at this region. We investigated the combined effect of allele and gene copy number of FCGR3A-158F/V and FCGR3B-NA1/NA2 on susceptibility to UC. Study subjects were composed of a total of 752 Japanese patients with UC and 2062 Japanese control subjects. To estimate allele copy number of the 2 polymorphisms, we integrated the results of PCR-based real-time Invader assay (PCR-RETINA) that measures the allelic ratio and Taqman assay that detects the total copy number. We analyzed the associations of allele copy number with UC using logistic regression model. Gene and allele copy numbers of FCGR3A and FCGR3B were successfully determined in more than 99.5% of the study subjects. Allele copy number of FCGR3A-158F/V demonstrated significant association with susceptibility to UC (P = 0.02), although each single-nucleotide polymorphism and copy number variation alone did not show significant association. Although allele copy number of FCGR3B-NA1/NA2 (P = 0.002) also showed significant association with UC susceptibility, this association seemed to reflect the effect of FCGR3B gene copy number. Subsequent haplotype analyses revealed a strong association of a haplotype FCGR2A-131H/R and copy number of FCGR3B gene (P = 6.5 × 10). Allele copy number of FCGR3A-158F/V and FCGR3B gene copy number were associated with UC susceptibility. Our results suggest that organizing handling of immune complex by FCGR3A, FCGR3B, and FCGR2A may play a crucial role in the pathogenesis of UC.
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impact of allele copy number of polymorphisms in fcgr3a and fcgr3b genes on susceptibility to ulcerative colitis
Inflammatory Bowel Diseases, 2013Co-Authors: Kouichi Asano, Junji Umeno, Naoya Hosono, Yutaka Kiyohara, Atsushi Hirano, Motohiro Esaki, Takayuki Matsumoto, Toshiyuki Matsui, Michiaki KuboAbstract:BACKGROUND Polymorphisms in the Fcγ receptor genes have been implicated in several autoimmune diseases, including ulcerative colitis (UC). However, most of these reports had not taken into account the effect of copy number variation at this region. METHODS We investigated the combined effect of allele and gene copy number of FCGR3A-158F/V and FCGR3B-NA1/NA2 on susceptibility to UC. Study subjects were composed of a total of 752 Japanese patients with UC and 2062 Japanese control subjects. To estimate allele copy number of the 2 polymorphisms, we integrated the results of PCR-based real-time Invader assay (PCR-RETINA) that measures the allelic ratio and Taqman assay that detects the total copy number. We analyzed the associations of allele copy number with UC using logistic regression model. RESULTS Gene and allele copy numbers of FCGR3A and FCGR3B were successfully determined in more than 99.5% of the study subjects. Allele copy number of FCGR3A-158F/V demonstrated significant association with susceptibility to UC (P = 0.02), although each single-nucleotide polymorphism and copy number variation alone did not show significant association. Although allele copy number of FCGR3B-NA1/NA2 (P = 0.002) also showed significant association with UC susceptibility, this association seemed to reflect the effect of FCGR3B gene copy number. Subsequent haplotype analyses revealed a strong association of a haplotype FCGR2A-131H/R and copy number of FCGR3B gene (P = 6.5 × 10). CONCLUSIONS Allele copy number of FCGR3A-158F/V and FCGR3B gene copy number were associated with UC susceptibility. Our results suggest that organizing handling of immune complex by FCGR3A, FCGR3B, and FCGR2A may play a crucial role in the pathogenesis of UC.
Raheleh Rahbari - One of the best experts on this subject based on the ideXlab platform.
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understanding the genomic structure of copy number variation of the low affinity fcγ receptor region allows confirmation of the association of fcgr3b deletion with rheumatoid arthritis
Human Mutation, 2017Co-Authors: Belinda Chihota, Hasret Ozturk, Sara Saleem, Eduardo Tarazonasantos, German Tischler, Luciana W. Zuccherato, Raheleh Rahbari, Lee MachadoAbstract:Fcγ receptors are a family of cell-surface receptors that are expressed by a host of different innate and adaptive immune cells and mediate inflammatory responses by binding the Fc portion of immunoglobulin G (IgG). In humans, five low affinity receptors are encoded by the genes FCGR2A, FCGR2B, FCGR2C, FCGR3A and FCGR3B, which are located in a 82.5kb segmental tandem duplication on chromosome 1q23.3, which shows extensive copy number variation. Deletions of FCGR3B have been suggested to increase the risk of inflammatory diseases such as systemic lupus erythematosus and rheumatoid arthritis. In this study we identify the deletion breakpoints of FCGR3B deletion alleles in the UK population and endogamous Native American populations, and show that some but not all alleles are likely to be identical-by-descent. We also localise a duplication breakpoint, confirming that the mechanism of CNV generation is non-allelic homologous recombination, and identify several alleles with gene conversion events using fosmid sequencing data. We use information on the structure of the deletion alleles to distinguish FCGR3B deletions from FCGR3A deletions in whole genome aCGH data. Reanalysis of published aCGH data supports association of FCGR3B deletion with increased risk rheumatoid arthritis in a large cohort of 1982 cases and 3271 controls (Odds Ratio 1.61, p=2.9x10-3).
