About InVivoSIM anti-human TNFα (Infliximab Biosimilar) This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Infliximab making it ideal for research use. This Infliximab biosimilar reacts with human TNFα (tumor necrosis factor-alpha) a multifunctional proinflammatory cytokine. TNFα exists as a soluble 17 kDa monomer, which forms homotrimers in circulation or as a 26 kDa membrane-bound form. TNFα belongs to the TNF superfamily of cytokines and signals through its two receptors, TNFR1 and TNFR2 which can be activated by both the soluble trimeric and membrane-bound and forms of TNFα. TNFα is primarily produced by macrophages in response to foreign antigens such as bacteria (lipopolysaccharides), viruses, and parasites as well as mitogens and other cytokines but can also be expressed by monocytes, neutrophils, NK cells, CD4 T cells and some specialized dendritic cells. TNFα is known to play key roles in a wide spectrum of biological processes including immunoregulation, cell proliferation, differentiation, apoptosis, antitumor activity, inflammation, anorexia, cachexia, septic shock, hematopoiesis, and viral replication. TNFα dysregulation has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Infliximab blocks the interaction of TNFα with the TNFR1 (p55) and TNFR2 (p75) resulting in a down-regulation of the inflammatory response associated with autoimmune diseases. InVivoSIM anti-human TNFα (Infliximab Biosimilar) Specifications IsotypeHuman IgG1 Recommended Isotype Control(s)RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer ImmunogenHuman TNFα Reported ApplicationsTNFα neutralization Flow Cytometry ELISA Western Blot FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<1EU/mg (<0.001EU/μg) Determined by LAL gel clotting assay Aggregation<5% Determined by SEC Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtration ProductionPurified from cell culture supernatant in an animal-free facility PurificationProtein A RRIDAB_2894727 Molecular Weight150 kDa StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoSIM anti-human TNFα (Infliximab Biosimilar) (CLONE: Infliximab)Zheng N, Fang J, Xue G, Wang Z, Li X, Zhou M, Jin G, Rahman MM, McFadden G, Lu Y (2022). "Induction of tumor cell autosis by myxoma virus-infected CAR-T and TCR-T cells to overcome primary and acquired resistance" Cancer Cell 40(9):973-985.e7. PubMedCytotoxicity of tumor-specific T cells requires tumor cell-to-T cell contact-dependent induction of classic tumor cell apoptosis and pyroptosis. However, this may not trigger sufficient primary responses of solid tumors to adoptive cell therapy or prevent tumor antigen escape-mediated acquired resistance. Here we test myxoma virus (MYXV)-infected tumor-specific T (TMYXV) cells expressing chimeric antigen receptor (CAR) or T cell receptor (TCR), which systemically deliver MYXV into solid tumors to overcome primary resistance. In addition to T cell-induced apoptosis and pyroptosis, tumor eradication by CAR/TCR-TMYXV cells is also attributed to tumor cell autosis induction, a special type of cell death. Mechanistically, T cell-derived interferon γ (IFNγ)-protein kinase B (AKT) signaling synergizes with MYXV-induced M-T5-SKP-1-VPS34 signaling to trigger robust tumor cell autosis. CAR/TCR-TMYXV-elicited autosis functions as a type of potent bystander killing to restrain antigen escape. We uncover an unexpected synergy between T cells and MYXV to bolster solid tumor cell autosis that reinforces tumor clearance.
