Anti-FCGR3B monoclonal antibody, clone G7 [FITC]

In this study, we aimed to investigate whether the distribution of the Fc gamma RIIa and Fc gamma RIIIb polymorphisms determines susceptibility to systemic lupus erythematosus (SLE) and acts as predictors of SLE clinical manifestations in the Brazilian patients. A total of 157 patients that fulfilled the American College of Rheumatology classification criteria for SLE and 160 healthy volunteers were included in this study. FCGR2A and FCGR3B genotypes were determined by polymerase chain reaction-based allotyping methods with allele-specific primers; the clinical features were obtained from the patients' official medical records. In the case of Fc gamma RIIa polymorphism, it was observed association of the allele FCGR2A-R-131 (p = 0.02, odds ratio (OR) = 1.44) and genotype RR-131 (p = 0.03, OR = 2.09) with SLE. These associations were higher with allele (p<0.01, OR = 1.67) as well genotype (p = 0.01, OR = 2.85) when lupus nephritis was considered. In contrast, the allele FCGR2A-H-131 was associated with susceptibility to arthritis and anti-DNA antibodies (p = 0.05 for both). As for Fc gamma RIIIb polymorphism, skewing did not differ significantly between patients and controls, however the genotype FCGR3B*02*02 was associated with susceptibility to arthritis (p = 0.02) and malar rash (p = 0.03), but no association with nephritis was found. The results demonstrate that Fc gamma RIIa polymorphism is associated with susceptibility to SLE in Brazilian patients, whereas for Fc gamma RIIIb polymorphism no association was found. However, notably, both polymorphisms present allelic variants that influence the clinical manifestations and may contribute to the pathogenesis of the disease. In addition, to our knowledge, this is the first study considering the frequency of Fc gamma RIIIb polymorphism in Brazilian SLE patients.

Anti-glomerular basement membrane antibody disease (anti-GBM disease) is a rare disorder characteristic of universally poor outcome. Fc gamma receptors (Fc gamma Rs) play important roles in anti-GBM disease based on evidence from animal models. Copy number variation (CNV) influences disease susceptibility. The Fc gamma Rs genes show CNV, and CNV of the FCGR3B gene is associated with glomerulonephritis in systemic lupus erythematosus and anti-neutrophil cytoplasmic antibody-associated small vasculitis. Here, we investigated CNV of three FCGR genes, including two (FCGR3A and FCGR3B) for activating Fc gamma Rs and one (FCGR2B) for inhibitory Fc gamma R by duplex quantitative real-time 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 = 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.