重组抗人CD16单克隆抗体(克隆号3G8) ，小鼠IgG1 Kappa | Syd Labs PA007331.m1

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抗人CD16抗体（3G8）参考文献:

1. Comparison of the different anti-CD16 antibody clones in the activation and expansion of peripheral blood NK cells
Jinho Kim,et al.Sci Rep. 2023.PMCID: PMC10258201
“Natural killer (NK) cells are promising tool for cancer treatment. Methods have been developed for large-scale NK cell expansion, including feeder cell-based methods or methods involving stimulation with NK cell activating signals, such as anti-CD16 antibodies. Different clones of anti-CD16 antibodies are available; however, a comprehensive comparison of their differential effects on inducing NK cell activation and expansion has not been conducted among these various clones under the same experimental conditions. Herein, we found that the NK cell expansion rate differed depending on the various anti-CD16 antibodies (CB16, 3G8, B73.1, and MEM-154) coated on microbeads when stimulated with genetically engineered feeder cells, K562‑membrane-bound IL‑18, and mbIL‑21 (K562‑mbIL‑18/-21). Only the CB16 clone combination caused enhanced NK cell expansion over K562‑mbIL‑18/-21 stimulation alone with similar NK cell functionality. Treatment with the CB16 clone once on the initial day of NK cell expansion was sufficient to maximize the combination effect. Overall, we developed a more enhanced NK expansion system by merging a feeder to effectively stimulate CD16 with the CB16 clone.”
2. Factor VIII moiety of recombinant Factor VIII Fc fusion protein impacts Fc effector function and CD16+ NK cell activation
H.A. Daniel Lagassé,et al.Front Immunol. 2024.PMCID: PMC11035769
“Recombinant Factor VIII-Fc fusion protein (rFVIIIFc) is an enhanced half-life therapeutic protein product used for the management of hemophilia A. Recent studies have demonstrated that rFVIIIFc interacts with Fc gamma receptors (FcγR) resulting in the activation or inhibition of various FcγR-expressing immune cells. We previously demonstrated that rFVIIIFc, unlike recombinant Factor IX-Fc (rFIXFc), activates natural killer (NK) cells via Fc-mediated interactions with FcγRIIIA (CD16). Additionally, we showed that rFVIIIFc activated CD16+ NK cells to lyse a FVIII-specific B cell clone. Here, we used human NK cell lines and primary NK cells enriched from peripheral blood leukocytes to study the role of the FVIII moiety in rFVIIIFc-mediated NK cell activation. Following overnight incubation of NK cells with rFVIIIFc, cellular activation was assessed by measuring secretion of the inflammatory cytokine IFNγ by ELISA or by cellular degranulation. We show that anti-FVIII, anti-Fc, and anti-CD16 all inhibited indicating that these molecules were involved in rFVIIIFc-mediated NK cell activation. To define which domains of FVIII were involved, we used antibodies that are FVIII domain-specific and demonstrated that blocking FVIII C1 or C2 domain-mediated membrane binding potently inhibited rFVIIIFc-mediated CD16+ NK cell activation, while targeting the FVIII heavy chain domains did not. We also show that rFVIIIFc binds CD16 with about five-fold higher affinity than rFIXFc. Based on our results we propose that FVIII light chain-mediated membrane binding results in tethering of the fusion protein to the cell surface, and this, together with increased binding affinity for CD16, allows for Fc-CD16 interactions to proceed, resulting in NK cellular activation. Our working model may explain our previous results where we observed that rFVIIIFc activated NK cells via CD16, whereas rFIXFc did not despite having identical IgG1 Fc domains.”
3. Multiplex interrogation of the NK cell signalome reveals global downregulation of CD16 signaling during lentivirus infection through an IL-18/ADAM17-dependent mechanism
Sho Sugawara,et al.PLoS Pathog. 2023.PMCID: PMC10503717
“Despite their importance, natural killer (NK) cell responses are frequently dysfunctional during human immunodeficiency virus-1 (HIV-1) and simian immunodeficiency virus (SIV) infections, even irrespective of antiretroviral therapies, with poorly understood underlying mechanisms. NK cell surface receptor modulation in lentivirus infection has been extensively studied, but a deeper interrogation of complex cell signaling is mostly absent, largely due to the absence of any comprehensive NK cell signaling assay. To fill this knowledge gap, we developed a novel multiplex signaling analysis to broadly assess NK cell signaling. Using this assay, we elucidated that NK cells exhibit global signaling reduction from CD16 both in people living with HIV-1 (PLWH) and SIV-infected rhesus macaques. Intriguingly, antiretroviral treatment did not fully restore diminished CD16 signaling in NK cells from PLWH. As a putative mechanism, we demonstrated that NK cells increased surface ADAM17 expression via elevated plasma IL-18 levels during HIV-1 infection, which in turn reduced surface CD16 downregulation. We also illustrated that CD16 expression and signaling can be restored by ADAM17 perturbation. In summary, our multiplex NK cell signaling analysis delineated unique NK cell signaling perturbations specific to lentiviral infections, resulting in their dysfunction. Our analysis also provides mechanisms that will inform the restoration of dysregulated NK cell functions, offering potential insights for the development of new NK cell-based immunotherapeutics for HIV-1 disease.”

Syd Labs抗人CD16单克隆抗体(克隆号3G8) ，小鼠IgG1 Kappa（货号：PA007331.m1）推荐同型对照抗体:

重组小鼠IgG1同型对照抗体

Syd Labs提供以下体内实验级重组抗人CD16, CD32和CD64单克隆抗体:

Recombinant Anti-human CD16 monoclonal antibody (Clone: 3G8)
Recombinant Anti-human CD32 monoclonal antibody (Clone: IV.3)
Recombinant Anti-human CD64 monoclonal antibody (Clone: H22)

Syd Labs提供以下体内实验级重组抗小鼠CD16, CD32和CD64单克隆抗体:

Recombinant Anti-mouse CD16/CD32 monoclonal antibody (Clone: 2.4G2)

Syd Labs提供以下重组抗人CD16, CD32和CD64单克隆抗体（流式细胞术用）:

Recombinant Anti-human CD16 monoclonal antibody (Clone: 3G8) for flow cytometry
Recombinant Anti-human CD32 monoclonal antibody (Clone: IV.3) for flow cytometry
Recombinant Anti-human CD64 monoclonal antibody (Clone: H22) for flow cytometry

请记住我们的产品信息: 重组抗人CD16单克隆抗体(克隆号3G8) ，小鼠IgG1 Kappa: PA007331.m1 Syd LabsRecombinant Anti-human CD16 Monoclonal Antibody (Clone: 3G8), Mouse IgG1 Kappa。