An antibody raised against the Fc fragment of IgG, low affinity IIIb, receptor FCGR3B low affinity immunoglobulin gamma Fc region receptor III-b isoform.
Catalogue number crb2005633 Antibody Anti-FCGR3B antibody Antigen Peptide KLH conjugated synthetic peptide crb1200840e Protein ID O75015 Human FCGR3B Aliases Low affinity immunoglobulin gamma Fc region receptor III-B, Low affinity immunoglobulin γ Fc region receptor III-B, Fc-gamma RIII-beta, Fc-gamma RIII-β, , Fc-gamma RIII, Fc-gamma RIIIb, FcRIII, FcRIIIb, FcR-10, IgG Fc receptor II Cross-Reactivity Human Target Protein Species Human Host Species Rabbit Antibody Type Polyclonal Concentration 1mg/ml Target FCGR3B Storage Stabilisers The product should be stored at -20°C for short term storage and long term storage. Avoid repeated freeze/ thaw cycles. Family Hominidae Storage The product should be stored at -20°C for short term storage and long term storage. Avoid repeated freeze/ thaw cycles. References
Rahbari et al., (2017). 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. Hum Mutat. 38(4): 390. PMID: 27995740.
Fc gamma receptors (FcγRs) are expressed on a host of different innate and adaptive immune cell-surfaces, including the leukocyte surface and interact with the Fc domain of immunoglobulin G (IgG) antibodies to mediate inflammatory responses.
Interaction of FcγRs with IgG immune complexes initiates intracellular signalling pathways that lead to a variety of either immunostimulatory or immunosuppressive downstream events, including cytokine/chemokine production. FcγRs are involved in modulating a range of processes, including antibody production, antigen presentation, and activation of B cells and innate immune effector cells.
In humans; five genes FCGR2A, FCGR2B, FCGR2C, FCGR3A, and FCGR3B, located in an 82.5‐kb segmental tandem duplication on chromosome 1q23.3, encode five low‐affinity receptors FcγRIIa, FcγRIIb, FcγRIIc, FcγRIIIa and FcγRIIIb. These genes have extensive copy‐number variation (CNV) and FcγR genetic variation can have significant implications on how the immune system reacts to different stimuli. Deletions of FCGR3B have been suggested to increase the risk of inflammatory diseases such as systemic lupus erythematosus and rheumatoid arthritis (RA).