Anti-FCGR2B monoclonal antibody [PE/Cy5.5®]

The determination of copy number variation (CNV) is very important for the evaluation of genomic traits in several species because they are a major source for the genetic variation, influencing gene expression, phenotypic variation, adaptation and the development of diseases. The aim of this study was to obtain a CNV genome map using the Illumina Bovine SNP50 BeadChip data of 651 bulls of the Italian Brown Swiss breed. PennCNV and SVS7 (Golden Helix) software were used for the detection of the CNVs and Copy Number Variation Regions (CNVRs). A total of 5,099 and 1,289 CNVs were identified with PennCNV and SVS7 software, respectively. These were grouped at the population level into 1101 (220 losses, 774 gains, 107 complex) and 277 (185 losses, 56 gains and 36 complex) CNVR. Ten of the selected CNVR were experimentally validated with a qPCR experiment. The GO and pathway analyses were conducted and they identified genes (false discovery rate corrected) in the CNVR related to biological processes, cellular component, molecular function and metabolic pathways. Among those, we found the FCGR2B, PPAR alpha, KATNAL1, DNAJC15, PTK2, TG, STAT family, NPM1, GATA2, LMF1, ECHS1 genes, already known in literature because of their association with various traits in cattle. Although there is variability in the CNVRs detection across methods and platforms, this study allowed the identification of CNVRs in Italian Brown Swiss, overlapping those already detected in other breeds and finding additional ones, thus producing new knowledge for association studies with traits of interest in cattle.

Data suggests that modulation of Fc gamma RIIB expression represents a significant risk factor for the development of autoimmunity. In this study, we investigated this notion in mice that possess genetics permissible for the development of autoimmunity. To this end, Mrl-MpJ Fcgr2b-/- mice were monitored for the development of autoreactivity. We found that Fc gamma RIIB deficiency led to chronic B cell activation associated with increased germinal center and plasma cell accumulation in the spleen. Likewise, Mrl-MpJ Fcgr2b-/- mice exhibited significant serum IgG reactivity against DNA. We further analyzed the IgG isotype contribution to the anti-dsDNA response and found increases in all subtypes with the exception of IgG3. In particular, we found large increases in IgG1 and IgG2b autoreactivity correlating with significant increases in immune complex deposition and kidney pathology. Finally, we found dendritic cells derived from Mrl-MpJ Fcgr2b-/- mice greatly increased IL-12 expression upon coincubation with apoptotic thymocytes compared with wild-type controls. The results indicate that Fc gamma RIIB is an important regulator of peripheral tolerance and attenuation of the inhibitory signal it provides enhances autoimmune disease on susceptible backgrounds. Additionally, the data indicates Fc gamma RIIB function has a significant impact on APC activity, suggesting a prominent role in dendritic cell activity in response to interaction with particulate autoantigens.