Anti tnfα xt3

Manufactured by BioXCell

Anti-TNFα (XT3.11) is a monoclonal antibody that binds to and neutralizes the proinflammatory cytokine Tumor Necrosis Factor-alpha (TNF-α). This antibody is commonly used in research applications to study the role of TNF-α in various biological processes and disease models.

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6 protocols using anti tnfα xt3

Immune Checkpoint Blockade and FMT in Mice

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Mice used were 6–7 weeks old at the start of experiments and gender-matched. Female mice were used in most experiments for this study. Mice treated with immune checkpoint blockade drugs were intraperitoneally administered anti-CTLA4 (9H10, BioXCell), using doses of 200 μg, and anti-PD-1, (RMP1-14, BioXCell) at a dose of 250 μg, once per week^{40 (link)}. All experimental mice were co-housed in specific pathogen–free facilities at King’s College London Biological Services Unit or Imperial Hammersmith CBS. Untreated control mice were housed in a separate box from CPI + FMT treated mice. Mice treated with depleting antibodies were intraperitoneally administered once a week, at the same time of giving anti-CTLA4 and anti-PD-1 antibodies, either 500 μg anti-TNFα (XT3.11, BioXCell), 500 μg anti-IFNγ (H22, BioXCell) or 150 μg anti-IL-23(p19) (G23-8, BioXCell). Control-isotype clones used were 2A3 (rat IgG2a) and HRPN (rat IgG1).

Lo J.W., Cozzetto D., Alexander J.L., Danckert N.P., Madgwick M., Knox N., Sieh J.Y., Olbei M., Liu Z., Ibraheim H., Blanco J.M., Kudo H., Seoane R.C., Possamai L.A., Goldin R., Marchesi J., Korcsmaros T., Lord G.M, & Powell N. (2023). Immune checkpoint inhibitor-induced colitis is mediated by polyfunctional lymphocytes and is dependent on an IL23/IFNγ axis. Nature Communications, 14, 6719.

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Immune Modulation in Tumor Models

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Mice were intraperitoneally (i.p.) injected with 200µg anti-CD8a (53-6.72, BioXcell), anti-CD4 (GK1.5, BioXcell), anti-NK1.1 (PK-136, BioXcell), anti-TNFα (XT3.11, BioXcell), anti-IFN (XMG1.2, BioXcell), anti-IL-17a (17F3, BioXcell) antibodies or IgG one day before tumor cell injection, and further the treatment was continued on days 2, 5, and 8 with 150µg antibodies. 1µg recombinant murine TNF (Peprotech) or vehicle were i.p. injected as above.

Uddin M.N., Zhang Y., Harton J.A., MacNamara K.C, & Avram D. (2014). TNFα-dependent hematopoiesis following Bcl11b deletion in T cells restricts etastatic melanoma. Journal of immunology (Baltimore, Md. : 1950), 192(4), 1946-1953.

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Blocking TNF-α and Lymphocyte Entry in RV Infection

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To block TNF‐α in vivo, mice were injected with 0.3 mg of anti‐TNF‐α (XT3.11; BioXcell) antibody intravenously on days 3 and 4 after RV infection. We used 100 μg/mouse InVivoMAb anti‐mouse L‐Selectin antibody (CD62L, clone Mel‐14, BioXcell) i.p. on day 4 post‐RV infection to block further entry of circulating lymphocytes into LNs without affecting lymphocyte egress from LNs. Control mice received PBS (Gibco).

Nakawesi J., Konjit G.M., Dasoveanu D., Johansson‐Lindbom B, & Lahl K. (2021). Rotavirus infection causes mesenteric lymph node hypertrophy independently of type I interferon or TNF‐α in mice. European Journal of Immunology, 51(5), 1143-1152.

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Enhancing Oncolytic Virus Therapy

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Cells were transfected with combinations of non-targeting (NT), Receptor Interacting Protein1 (RIP1), Caspase-8 (CASP8), TNF-R1, and DR5 small interfering RNA (siRNA) (ON-Target SmartPool, Thermo Fisher Scientific) for 48 hr. Cells were then treated with vehicle or 5 μM LCL161 and infected with the indicated OV. Cell viability was assessed by Alamar blue. Knockdown of TNF-R1 and DR5 was determined by western blotting using the following antibodies: RIP1 (D94C12; Cell Signaling Technology), CASP8 (AF705), DR5 (3696; Cell Signaling Technology), TNF-R1 (3736; Cell Signaling Technology), β-tubulin (E7; Developmental Studies Hybridoma Bank), and GAPDH (GAPDH-71.1; Sigma). For antibody-mediated neutralization of TNF-α, cells were treated with 50 μg/mL of mouse immunoglobulin G (IgG) control (HRPN; BioXCell) or anti-TNF-α (XT3.11; BioXCell). One hour later, cells were treated with vehicle or 5 μM LCL161 and the indicated MOI of OV. Cell viability was assessed by Alamar blue.

Beug S.T., Pichette S.J., St-Jean M., Holbrook J., Walker D.E., LaCasse E.C, & Korneluk R.G. (2018). Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression. Molecular Therapy Oncolytics, 10, 28-39.

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Modulating Immune Responses in Mice

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For depletion of CD8⁺ T cells and neutralization of cytokines, starting at 21dpi, mice were intraperitoneally administered 20μg or 500μg of anti-CD8 Ab (53–6.7 and 2.43; BioXCell), anti-IL-1β (B122; BioXCell), anti-IFNγ (XMG1.2; BioXCell), anti-TNFα (XT3.11; BioXCell) or isotype control immunoglobulin G (IgG) in 200μL of phosphate-buffered saline (PBS) once a week. Mice were euthanized 3 days after the last treatment.

Narasimhan H., Cheon I.S., Qian W., Hu S., Parimon T., Li C., Goplen N., Wu Y., Wei X., Son Y.M., Fink E., Santos G., Tang J., Yao C., Muehling L., Canderan G., Kadl A., Cannon A., Young S., Hannan R., Bingham G., Arish M., Chaudhari A.S., Sturek J., Pramoonjago P., Shim Y.M., Woodfolk J., Zang C., Chen P, & Sun J. (2023). Proximal immune-epithelial progenitor interactions drive chronic tissue sequelae post COVID-19. Research Square.

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Imiquimod-Induced Skin Inflammation Model

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Mice received a daily topical dose of 25 mg of commercially available imiquimod cream (5%) (Beselna Cream, Mochida Pharmaceutical) on the right ear for 10 days, with the exception of day 5 or 6. For blockade experiments, a control antibody or an anti–IL-6 (MP5-20F3), anti–TNF-α (XT3.11), or anti–IFN-γ (XMG1.2) monoclonal antibody (BioXCell) was administered on 2 consecutive days, followed by no treatment on the third day for 10 days at 400 μg/dose via i.p. injection. Mice received 6 total injections. Baricitinib (AdooQ BioScience) was administered daily by oral gavage at 10 mg/kg/dose for 10 days, with the exception of day 5.

Sasaki Y., Arimochi H., Otsuka K., Kondo H., Tsukumo S.I, & Yasutomo K. (2022). Blockade of the CXCR3/CXCL10 axis ameliorates inflammation caused by immunoproteasome dysfunction. JCI Insight, 7(7), e152681.

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