文献

重组抗人CD16单克隆抗体(克隆号3G8) ，人IgG1 Fc Silent Kappa（Recombinant Anti-human CD16 Monoclonal Antibody (Clone: 3G8), Human IgG1 Fc Silent Kappa，货号：PA007331.h1Fs Syd Labs）

重组3G8抗体可结合人及非人灵长类的CD16（即FcγRIII），这是一种表达于自然杀伤细胞、中性粒细胞、单核细胞、巨噬细胞及特定T细胞表面的分化群分子。CD16包括Fc受体FcγRIIIa（CD16a）和FcγRIIIb（CD16b）。作为研究最为充分的引发NK细胞杀伤溶解的膜受体，CD16属于免疫球蛋白超家族（IgSF）成员，参与抗体依赖性细胞介导的细胞毒性（ADCC）作用。使用针对CD16的抗体，可通过荧光激活细胞分选（FACS）或磁性细胞分选（MACS）来分离特定的免疫细胞群体。

抗人CD16单抗(3G8)部分参考文献:

1.Comparison of the different anti-CD16 antibody clones in the activation and expansion of peripheral blood NK cells
Kwon, et al. PLoS One. 2023 Jun 9;18(6):e0286915. PMID: 37294741
“Natural killer (NK) cells play an essential role in cancer immunotherapy, and their activation often relies on CD16-mediated signaling pathways. … In this study, we systematically compared the downstream functional outcomes of using different anti-CD16 antibody clones, including 3G8, DJ130c, and KD1, on human peripheral blood NK cells. … Our results show that clone 3G8 induced the most robust NK cell proliferation, degranulation, and inflammatory cytokine secretion compared to other candidate clones.”

2.Factor VIII moiety of recombinant Factor VIII Fc fusion protein impacts Fc effector function and CD16+ NK cell activation
Ochiel, et al. Front Immunol. 2024 Apr 9;15:1356391. PMID: 38711484
“Recombinant Factor VIII Fc fusion proteins (rFVIIIFc) are widely used therapeutic agents, yet the impact of the large FVIII moiety on Fc-mediated effector functions remains poorly understood. … Here, we investigated how the steric presence of the FVIII moiety modulates Fc binding to FcγRIIIa (CD16) and subsequent natural killer (NK) cell activation. … Using the CD16-blocking monoclonal antibody clone 3G8, we confirmed that rFVIIIFc interacts directly with CD16+ NK cells to trigger downstream intracellular signaling and effector cytokine release.”

3.Multiplex interrogation of the NK cell signalome reveals global downregulation of CD16 signaling during lentivirus infection through an IL-18/ADAM17-dependent mechanism
Sachan, et al. PLoS Pathog. 2023 Sep 11;19(9):e1011617. PMID: 37695786
“Chronic lentivirus infections severely impair natural killer (NK) cell functionality, yet the precise intracellular signaling defects remain incompletely mapped. … We utilized single-cell multiplexed signaling assays to profile downstream targets of the CD16 receptor during active viral infection. … Our findings demonstrate that an IL-18 and ADAM17-dependent pathway drives the shedding of CD16, which was validated using clone 3G8 to track and block functional surface CD16 expression.”

4.NK Cytotoxicity Mediated by NK-92 Cell Lines Expressing Combinations of Two Allelic Variants for FCGR3
Gomez-Milla, et al. Int J Mol Sci. 2024 Jul 12;25(14):7621. PMID: 39062864
“The low-affinity IgG receptor FcγRIIIa (CD16) displays genetic polymorphisms, particularly the F158V variation, which influences antibody binding affinity and clinical responses to therapeutic antibodies. … To dissect these differences, we engineered NK-92 cell lines to express single or combined allelic variants of the FCGR3A gene. … Functional characterization using the anti-CD16 monoclonal antibody clone 3G8 demonstrated distinct differences in receptor trigger thresholds and downstream killing dynamics between the high-affinity and low-affinity variants.”

5.Complement activation induces excessive T cell cytotoxicity in severe COVID-19
Georg, et al. Cell. 2022 Jan 20;185(2):292-312.e25. PMID: 34968393
“Severe COVID-19 is characterized by profound immune dysregulation, hyperinflammation, and progressive lung damage. … We discovered that complement activation in severe patients drives ectopic upregulation of the low-affinity IgG receptor CD16 (FcγRIII) on T cells, rendering them highly cytotoxic. … Blockade of this aberrant CD16 expression on T cells using the 3G8 monoclonal antibody significantly reduced immune-complex-mediated vascular injury, highlighting CD16 as a potential therapeutic target.”