| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Low affinity immunoglobulin gamma Fc region receptor III-A, CD16a antigen, Fc-gamma RIII-alpha, Fc-gamma RIII, Fc-gamma RIIIa, FcRIII, FcRIIIa, FcR-10, IgG Fc receptor III-2, CD16a, FCGR3A, CD16A, FCG3, FCGR3, IGFR3 |
| Entrez GeneID | 2214 |
| WB Predicted band size | 29.1kDa |
| Host/Isotype | Mouse IgG1 |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | This FCGR3A antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 60-88 amino acids from human FCGR3A. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是3篇与FCGR3A抗体相关的文献摘要信息：
1. **文献名称**: *"Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcγRIIIa gene"*
**作者**: Cartron G et al.
**摘要**: 研究FCGR3A基因多态性(V158F)对利妥昔单抗治疗非霍奇金淋巴瘤疗效的影响，发现携带高亲和力V/V基因型的患者客观缓解率显著高于F/F型，提示FCGR3A多态性可作为生物标志物。
2. **文献名称**: *"FCGR3A and FCGR2A polymorphisms and their clinical relevance in patients with chronic lymphocytic leukemia treated with anti-CD20 monoclonal antibodies"*
**作者**: Weng WK et al.
**摘要**: 分析慢性淋巴细胞白血病患者接受奥法木单抗治疗时FCGR3A多态性与预后的关联，发现V/V基因型患者的总生存期更长，强调Fcγ受体基因型在单抗疗法中的重要性。
3. **文献名称**: *"FcγRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell FcγRIIIa, independently of the FcγRIIIa-48L/R/H phenotype"*
**作者**: Dall’Ozzo S et al.
**摘要**: 通过体外实验验证FCGR3A基因V158F突变会降低自然杀伤细胞对IgG1抗体的亲和力，进而影响ADCC效应，为优化抗体药物设计提供机制依据。
4. **文献名称**: *"Fcγ receptors as regulators of immune responses"*
**作者**: Nimmerjahn F, Ravetch JV
**摘要**: 综述性文献，系统阐述FCGR3A等Fcγ受体在调控抗体介导的免疫反应(如ADCC、细胞因子释放)中的核心作用，并讨论其在治疗性抗体开发中的靶向潜力。
FCGR3A (Fc gamma receptor IIIA), also known as CD16a, is a cell-surface receptor belonging to the immunoglobulin superfamily. It is primarily expressed on natural killer (NK) cells, macrophages, and dendritic cells. As a low-affinity receptor for the Fc region of IgG antibodies, FCGR3A plays a critical role in bridging innate and adaptive immunity by mediating antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis. These processes are essential for eliminating pathogens and malignant cells.
Therapeutically, FCGR3A is a key target in monoclonal antibody (mAb) therapies, such as rituximab and trastuzumab, which rely on Fc-FCGR3A interactions to recruit NK cells for tumor cell lysis. Genetic polymorphisms in FCGR3A, particularly the single nucleotide polymorphism (SNP) at position 158 (V/F), influence receptor affinity for IgG subtypes, impacting clinical outcomes in cancer and autoimmune treatments. For example, the FCGR3A-158V variant exhibits higher binding affinity, correlating with enhanced ADCC efficacy and better patient responses.
Dysregulation of FCGR3A signaling is implicated in autoimmune disorders (e.g., systemic lupus erythematosus) and infectious diseases, highlighting its dual role in immune regulation and pathology. Research continues to explore FCGR3A-targeted therapies, including engineered antibodies with optimized Fc domains and bispecific antibodies, to improve precision in immune modulation. Its pivotal role in immune effector functions makes FCGR3A a cornerstone in both understanding disease mechanisms and developing next-generation immunotherapies.
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