抗小鼠CD40单克隆抗体(克隆号FGK4.5) ，体内实验级重组，大鼠IgG2a Kappa | Syd Labs PA007274.r2a

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抗小鼠CD40单抗（FGK4.5）参考文献:

1. CD40 signaling restricts RNA virus replication in macrophages, leading to rapid innate immune control of acute virus infection
Kai J. Rogers,et al.J Leukoc Biol. 2021.PMCID: PMC7774454
“Many acute viral infections target tissue macrophages, yet the mechanisms of macrophage-mediated control of viruses are poorly understood. Here, we report that CD40 expressed by peritoneal macrophages restricts early infection of a broad range of RNA viruses. Loss of CD40 expression enhanced virus replication as early as 12–24 hours of infection and, conversely, stimulation of CD40 signaling with an agonistic antibody blocked infection. With peritoneal cell populations infected with the filovirus, wild-type (WT) Ebola virus (EBOV), or a BSL2 model virus, recombinant vesicular stomatitis virus encoding Ebola virus glycoprotein (rVSV/EBOV GP), we examined the mechanism conferring protection. Here we demonstrate that restricted virus replication in macrophages required CD154/CD40 interactions which stimulated IL-12 production through TRAF6-dependent signaling. In turn, IL-12 production resulted in interferon gamma (IFN-γ) production, which induced proinflammatory polarization of macrophages, protecting the cells from infection. These CD40-dependent events protected mice against virus challenge. CD40−/− mice were exquisitely sensitive to intraperitoneal challenge with a dose of rVSV/EBOV GP that was sublethal to CD40+/+ mice, exhibiting viremia within 12 hours of infection and rapidly succumbing to infection. This study identifies a previously unappreciated role for macrophage-intrinsic CD40 signaling in controlling acute virus infection.”
2. Mechanisms of CD40-dependent cDC1 licensing beyond costimulation
Renee Wu,et al.Nat Immunol. 2022.PMCID: PMC9896965
“CD40 signaling in classical type 1 dendritic cells (cDC1s) is required for CD8 T cell-mediated tumor rejection, but the underlying mechanisms are incompletely understood. Here, we identified CD40-induced genes in cDC1s, including Cd70, Tnfsf9, Ptgs2 and Bcl2l1, and examined their contributions to anti-tumor immunity. cDC1-specific inactivation of CD70 and COX-2, and global CD27 inactivation, only partially impaired tumor rejection or tumor-specific CD8 T cell expansion. Loss of 4-1BB, alone or in Cd27−/− mice, did not further impair anti-tumor immunity. However, cDC1-specific CD40 inactivation reduced cDC1 mitochondrial transmembrane potential and increased caspase activation in tumor-draining lymph nodes, reducing migratory cDC1 numbers in vivo. Similar impairments occurred during in vitro antigen presentation by Cd40−/− cDC1s to CD8+ T cells, which were reversed by re-expression of Bcl2l1. Thus, CD40 signaling in cDC1s not only induces costimulatory ligands for CD8+ T cells but also induces Bcl2l1 that sustains cDC1 survival during priming of anti-tumor responses.”
3. Macrophages and CD8+ T cells mediate the antitumor efficacy of combined CD40 ligation and imatinib therapy in gastrointestinal stromal tumors
Jennifer Q. Zhang,et al.Cancer Immunol Res. 2018.PMCID: PMC6203303
“Tyrosine kinase inhibition of gastrointestinal stromal tumors (GIST) is effective but typically culminates in resistance and is rarely curative. Immunotherapy has potential application to GIST, as we previously showed that T-cell checkpoint blockade increases the antitumor effects of imatinib. Here, we showed that ligation of CD40 using an agonistic antibody (anti-CD40) activated tumor-associated macrophages (TAMs) in vivo in a knock-in mouse model of GIST harboring a germline mutation in Kit exon 11. Activated TAMs had greater TNF production and NFκB signaling and directly inhibited tumor cells in vitro. Anti-CD40 required concomitant therapy with imatinib for efficacy and depended on TAMs, and to a lesser extent CD8+ T cells, but not on CD4+ T cells or B cells. In an analysis of 50 human GIST specimens by flow cytometry, we found that CD40 was expressed on human TAMs and tumor cells yet was downregulated after response to imatinib. CD40 ligation did not have a direct inhibitory effect on human GIST cells. Our findings provide the rationale for combining anti-CD40 and tyrosine kinase inhibition to treat human GIST.”

Syd Labs抗小鼠CD40重组抗体（克隆号FGK4.5），大鼠IgG2a Kappa（货号：PA007274.r2a）推荐同型对照抗体:

重组大鼠IgG2a同型对照抗体，体内实验级（In vivo Grade Recombinant Rat IgG2a Isotype Control Antibody）

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