Anti-Mouse IFNα [Clone TIF-3C5] — Purified in vivo PLATINUM™ Functional Grade

Clone TIF-3C5 is most commonly used in vivo in mice as a neutralizing antibody to block endogenous mouse interferon-alpha (IFNα), allowing researchers to study the biological and antiviral roles of IFNα during viral infections and immune responses.

Key in vivo applications in mice include:

• Neutralization of mouse IFNα: TIF-3C5 specifically recognizes and binds to several murine IFNα subtypes (IFN-αA, -1, -4, -5, -11, and -13) but does not bind IFNγ or IFNβ, enabling selective blockade of IFNα without affecting other type I interferons.
• Investigation of IFNα’s antiviral functions: By blocking IFNα in vivo, TIF-3C5 helps define the contribution of this cytokine to viral clearance and host protection during infections such as chikungunya virus (CHIKV), lymphocytic choriomeningitis virus (LCMV), dengue virus (DENV), and others.
• Dissection of immune and inflammatory responses: The antibody is used to analyze how IFNα signaling shapes cytokine production, immune cell recruitment, and overall pathogenesis, thereby distinguishing the functions of IFNα from IFNβ in vivo.
• Preclinical studies on immunopathology: In mouse models, TIF-3C5 blockade has been used to demonstrate that loss of IFNα signaling results in increased viral load, dissemination, and worsened clinical outcomes, reinforcing its key protective role.

Additional details:

• TIF-3C5 is purified with low endotoxin levels, making it suitable for in vivo administration without inducing off-target immune responses.
• The antibody has also been employed to study non-redundant functions of IFNα versus IFNβ by selectively blocking each cytokine in genetically modified mice.

Overall, TIF-3C5 is a standard tool for in vivo functional blockade of mouse IFNα, routinely applied in infectious disease, immunology, and inflammation research where dissecting type I interferon biology is critical.

Commonly used antibodies or proteins employed with TIF-3C5 (a monoclonal antibody targeting murine IFN-α) in the literature include:

• HDβ-4A7: This antibody specifically neutralizes murine IFN-β and is commonly used alongside TIF-3C5 to differentiate the roles of IFN-α versus IFN-β in experimental models.
• MAR1-5A3: An anti-IFNAR1 (type I interferon receptor) monoclonal antibody, frequently used in parallel with TIF-3C5 to achieve blockade of signaling from all type I interferons (both IFN-α and IFN-β) by blocking their shared receptor.
• Isotype control antibodies: These are non-specific control antibodies matching the isotype of TIF-3C5, used to confirm that any observed effects are due to specific binding rather than general immunoglobulin effects.

Experimental context:

• These antibodies are often used together in studies investigating the distinct roles of type I interferons (IFN-α vs. IFN-β) or to fully block type I IFN signaling in murine models, including infection (e.g., with West Nile virus), autoimmunity, and cancer immune response studies.
• TIF-3C5 is specific to IFN-α and does not bind murine IFN-β or IFN-γ, so HDβ-4A7 (for IFN-β) and MAR1-5A3 (for IFNAR1) are essential for direct comparison or comprehensive blockade.

Summary Table

References for these pairings and their experimental deployment:

• uses TIF-3C5, HDβ-4A7, and MAR1-5A3 to dissect type I IFN biology.
• notes MAR1-5A3 is often used with TIF-3C5 for comprehensive inhibition of type I IFNs.
• describes experiments directly comparing TIF-3C5 (IFN-α-specific blockade) with MAR1-5A3.

Other proteins, such as cytokines (e.g., IFN-γ) or genetically modified mice (e.g., IFNAR or IRF7 knockouts), are sometimes studied in parallel with these antibodies to further dissect signaling pathways, but the most common reagents paired with TIF-3C5 are the antibodies listed above.

Clone TIF-3C5 is a monoclonal antibody widely used in scientific research to specifically neutralize mouse interferon-alpha (IFN-α), and its key findings in the literature can be summarized as follows:

• Specificity and Selectivity: TIF-3C5 binds specifically to several murine IFN-α subtypes (e.g., IFN-αA, -1, -4, -5, -11, -13), but it does not bind murine IFN-β or IFN-γ. This makes it a valuable tool for dissecting the individual roles of IFN-α in immune responses.

• Functional Role in Viral Infection Models:

  • TIF-3C5 neutralizes the antiviral activity of IFN-α in vitro and in vivo, allowing researchers to study the effects of IFN-α deficiency.
  • In West Nile Virus (WNV) infection models, administration of TIF-3C5 significantly increased mice's susceptibility and lethality, mimicking the phenotype of IFN-α-deficient or IRF7-knockout mice. This demonstrates a key antiviral role for IFN-α during acute viral infection.
  • The lethality enhancement was statistically significant when TIF-3C5 was delivered using a regimen of three administrations (compared to two), and the increased lethality was observed in both wild-type and IFN-β-deficient mice.

• Role in Autoimmune and Inflammatory Models:

  • TIF-3C5 has been used to selectively ablate IFN-α activity in mouse models of type 1 diabetes, allowing for dissection of IFN-α’s specific contributions to pathogenesis distinct from other type I interferons.
  • In checkpoint immunotherapy studies, anti-IFNα (TIF-3C5) was used to investigate the role of IFN-α signaling in immune modulation and cancer therapy, although the blockade of IFNα did not always lead to improved immune or disease outcomes in certain settings, highlighting the context-dependent effects of type I IFNs.

• Tool for Dissecting Type I Interferon Biology:

  • By differentiating between IFN-α and IFN-β effects, TIF-3C5 has shown that these cytokines can have distinct, sometimes non-redundant roles in antiviral defense, immune regulation, and inflammation.
  • The neutralizing activity of TIF-3C5 against different IFN-α subtypes varies in potency, which may reflect differences in either binding affinity or the intrinsic activities of the individual subtypes.

• Technical Applications:

  • TIF-3C5 is used in functional assays (in vitro and in vivo), ELISA, Western blotting, and as a neutralizing antibody in experimental animal models.
  • It is manufactured to high purity with low endotoxin levels, suitable for sensitive in vivo studies.

In summary: TIF-3C5 has enabled researchers to define the exclusive contributions of IFN-α (versus IFN-β or IFN-γ) in murine models of infection, autoimmunity, and cancer, confirming that IFN-α is crucial for antiviral defense and that its blockade can shift disease outcomes in ways reminiscent of genetic IFN-α deficiency.

Should you need citations for specific disease models, mechanisms, or application protocols, please specify your area of interest.

Dosing regimens of clone TIF-3C5, an anti-mouse IFN-α monoclonal antibody, differ across mouse models depending on the disease context and experimental design, with doses typically ranging from 250 μg to 1 mg per injection and varying in number and timing of administrations within infection or tumor models. The most thoroughly documented regimens include single or multiple intraperitoneal (i.p.) injections, with precise timing tailored to the model and scientific question.

Key details from published studies include:

• West Nile Virus Infection Models:
  • Wild-type and knockout mice:
    • 500 μg TIF-3C5 i.p. one day prior and two days after infection, or
    • 250 μg TIF-3C5 i.p. one day prior, one day after, and three days after infection.
    • The three-dose, lower-mass regimen produced a more pronounced biological effect than the two-dose, higher-mass regimen.
• Cancer Immunotherapy Models (e.g., AE17, AB1, Renca):
  • 1 mg TIF-3C5 i.p., administered every third day for a total of three doses, starting three days after the initial immune checkpoint blockade (ICB) treatment.
• Chikungunya Virus Infection Models:
  • Wild-type mice were given 1 mg anti-mouse IFN-α (TIF-3C5) i.p. consistently, typically as a single dose, with direct comparison to IFN-β blockade and isotype controls.
• General Manufacturer Recommendations:
  • Leinco, a major supplier, notes that regimens vary and are adjusted based on disease model, mouse strain, experimental timing, and desired pharmacodynamic effect. Reported regimens typically fall within 250 μg–1 mg per injection, often repeated every 2–3 days during the early phase of infection or therapeutic intervention.

Adjustments are often made for:

• Mouse strain (e.g., wild-type vs. knockout).
• Disease type and severity.
• Timing relative to infection or therapy initiation.
• Desired depth and duration of IFN-α blockade.

In summary: while common regimens range from 250 μg to 1 mg per dose administered i.p., precise protocols are customized to the disease model and experiment, mainly varying in dose, number, and spacing of injections.