Anti-Mouse IFNAR-1 [Clone MAR1-5A3] — Purified in vivo GOLD™ Functional Grade

Anti-Mouse IFNAR-1 [Clone MAR1-5A3] — Purified in vivo GOLD™ Functional Grade

Product No.: I-401

[product_table name="All Top" skus="I-401"]

- -
- -
Clone
MAR1-5A3
Target
IFNAR1
Formats AvailableView All
Product Type
Monoclonal Antibody
Alternate Names
CD118, Ifar, Ifnar, Ifrc, INF-a receptor, Interferon-α/β receptor α chain precursor
Isotype
Mouse IgG1
Applications
B
,
ELISA
,
FC
,
in vivo
,
IP
,
WB

- -
- -
Select Product Size

Data

- -
- -

Antibody Details

Product Details

Reactive Species
Mouse
Host Species
Mouse
Recommended Dilution Buffer
Immunogen
This antibody was produced by In vivo genetic immunization of IFNAR1 knockout mice with a plasmid encoding the extracellular domain of murine IFNAR1.
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
< 1.0 EU/mg as determined by the LAL method
Purity
≥95% monomer by analytical SEC
>95% by SDS Page
Formulation
This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
Product Preparation
Functional grade preclinical antibodies are manufactured in an animal free facility using in vitro cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.
Storage and Handling
Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.
Country of Origin
USA
Shipping
Next Day 2-8°C
Applications and Recommended Usage?
Quality Tested by Leinco
FC The suggested concentration for clone MAR1-5A3 antibody for staining cells in flow cytometry is ≤ 2.0 μg per 106 cells in a volume of 100 μl or 100μl of whole blood. Titration of the reagent is recommended for optimal performance for each application. NOTE: Leinco Technologies suggests using Anti-Mouse IFNAR1-Biotin (With Streptavidin - PE; Part No. S211) (Leinco Product No.: I-402) for flow cytometry of mouse cells
Additional Applications Reported In Literature ?
B Clone MAR1-5A3 has a short half-life due to the rapid recycling of cells that express the IFNAR1 receptor. In order to block function In vivo, continual blocking of all compartments is necessary. Therefore, a large loading dose is necessary to saturate all In vivo binding sites and should be maintained to ensure binding site saturation. For In vivo blocking studies, a loading dose of 2.5 mg/mouse, followed by a weekly dose of 0.5 mg/mouse is recommended. The half-life following a 2.5 mg loading dose is approximately 5 days. However, if you fail to saturate the binding sites by injecting a low dose of 250 μg, for example, the half life is only 1.5 days.
WB For Western blotting, the suggested use of this reagent is 1.0 µg per ml (See Data Results) IP
ELISA
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
Clone MAR1-5A3 recognizes an epitope on mouse IFNAR1.
Background
IFNAR1 is a type I membrane protein, that in conjunction with IFNAR2, makes up the heterodimeric receptor that binds all type I IFNs, which includes IFN α and β. Binding and activation of the receptor stimulates Janus protein kinases, which leads to the phosphorylation of several other proteins, namely STAT1 and STAT2. IFNAR1 has also been shown to interact with PRMT1 and Tyrosine kinase 2. Type I IFNs are a family of cytokines that have been shown to promote anti-viral, anti-microbial, anti-tumor and autoimmune responses In vivo.
Antigen Distribution
IFNAR1 and IFNAR2 are coexpressed on nearly all cells.
Ligand/Receptor
IFN-α/β
PubMed
NCBI Gene Bank ID

Leinco Antibody Advisor

Powered by AI: AI is experimental and still learning how to provide the best assistance. It may occasionally generate incorrect or incomplete responses. Please do not rely solely on its recommendations when making purchasing decisions or designing experiments.

Clone MAR1-5A3 is used in in vivo mouse studies to functionally block type I interferon (IFN) receptor signaling by targeting the IFNAR-1 (interferon alpha/beta receptor subunit 1) on mouse cells without depleting the cells that express it.

Key details:

  • Mechanism: MAR1-5A3 is a monoclonal antibody that binds specifically to mouse IFNAR-1, a key part of the heterodimeric type I IFN receptor complex (IFNAR-1/IFNAR-2). This prevents type I IFNs (IFN-? and IFN-?) from binding their receptor, thereby blocking downstream signaling and the induction of interferon-stimulated genes (ISGs).
  • Typical use: It is administered to mice to create a transient and systemic blockade of type I IFN responses, allowing researchers to study the effects of type I IFN signaling deficiency in various physiological or disease models, such as viral infection, cancer, or autoimmune conditions.
  • Administration and dosing: A loading dose is required to saturate all in vivo IFNAR1 binding sites, followed by maintenance dosing due to rapid receptor recycling; for example, studies mention 200?µg every three days or a protocol of 2.5?mg/mouse followed by 0.5?mg/mouse weekly.
  • Non-depleting: MAR1-5A3 blocks receptor function without causing cell depletion because it is typically used as mouse IgG1, which, unlike other isotypes, does not mediate antibody-dependent cellular cytotoxicity or complement activation.

Summary of applications:

  • Used to mimic a type I IFN receptor knockout in wild-type mice.
  • Investigates the role of type I IFN signaling in immune response, pathogen defense, tumor immunity, and autoimmunity.
  • Often preferred for temporal and reversible abrogation versus permanent gene deletion.

Special notes:

  • Recombinant versions (e.g., MAR1-5A3-CP056) have been engineered (IgG2a isotype, Fc silenced) to further reduce any potential for effector functions, paralleling therapeutic anti-IFNAR1 antibodies.
  • The antibody requires regular dosing because of the turnover and recycling of IFNAR-expressing cells; this ensures consistent blockade.

Commonly used antibodies and proteins in the literature alongside MAR1-5A3 include other monoclonal antibodies targeted at interferon signaling components, isotype controls, and antibodies against viral or cellular proteins relevant to the specific experimental context.

Key examples include:

  • Isotype controls: Frequently used are IgG2a mAb (2H2) against dengue virus prM protein, GIR-208, and PIP as controls to MAR1-5A3, ensuring experimental specificity.
  • Other interferon pathway antibodies: TIF-3C5 and HDβ-4A7 are cited as antibodies blocking or detecting interferon alpha or beta, used in experiments to compare with or complement MAR1-5A3's effects.
  • Related receptor antibodies: Since IFNAR-1 and IFNAR-2 form a heterodimeric receptor complex, studies may also utilize antibodies targeting IFNAR-2 to explore the full signaling blockade.
  • Cellular marker antibodies: Depending on the study focus (e.g., immunophenotyping after IFNAR blockade), antibodies against immune cell surface markers (CD3, CD4, CD8, CD45, etc.) are often used together for flow cytometry or functional assays.
  • Other cytokine or viral protein antibodies: In viral infection models, coworkers such as anti-dengue virus prM protein are used for viral detection or quantification.

Additional details:

  • MAR1-5A3 is commonly paired with isotype controls in blocking or depletion experiments for unbiased functional assessment.
  • Recombinant or chimeric forms of MAR1-5A3 (e.g., MAR1-5A3-CP056) are available to enable specific functional studies with modified Fc regions for decreased effector functions (preventing ADCC/CDC), which may be co-used with other immune-modulatory antibodies.

In summary, MAR1-5A3 is typically used alongside control antibodies, complementary interferon-targeting clones (such as anti-IFN-?), and standard immunological markers, all tailored to the experimental design and hypothesis.

The monoclonal antibody clone MAR1-5A3 is widely cited in scientific literature for its role as a blocking antibody against mouse type I interferon receptor (IFNAR1), enabling experimental manipulation of interferon signaling in vivo. Key findings from studies citing MAR1-5A3 cover its central use in dissecting the immune response, developing infection models, and understanding pathogenesis mechanisms.

Key findings:

  • Mechanism and Specificity: MAR1-5A3 binds to the extracellular domain of mouse IFNAR1, blocking type I interferon (IFN-α/β) signaling, which is central to innate antiviral, antimicrobial, antitumor, and autoimmune responses.

  • Immune Modulation: Blocking IFNAR1 with MAR1-5A3 enhances certain aspects of humoral immunity. In particular, it increases the generation of T follicular helper (T_FH) cells, germinal center (GC) B cells, and plasma cells during chronic viral infection (e.g., lymphocytic choriomeningitis virus, LCMV). This blockade results in higher virus-specific antibody levels, demonstrating that type I IFN signaling restrains aspects of the antiviral humoral response.

  • Infection Models and Disease Susceptibility: MAR1-5A3 is crucial for creating mouse models permissive to flavivirus infection (e.g., Zika virus, West Nile virus, Usutu virus, dengue virus) in otherwise resistant wild-type mice. Key findings here:

    • Pre-treatment with MAR1-5A3 leads to enhanced viral replication, increased viremia, and in some cases, lethal disease, mimicking immunodeficient mouse phenotypes.
    • The route, dose, and timing of antibody administration can modulate disease severity.
    • Pathogenic outcomes depend on factors such as viral strain, dose, mouse age, and route of inoculation.
    • MAR1-5A3 does not efficiently cross the blood brain barrier, so observed neurovirulence after infection is likely due to enhanced systemic infection and CNS invasion by the virus.
  • Technical Considerations: MAR1-5A3 administration is transient, non-cell-depleting, and has a defined half-life (around 5.2 days in wild-type mice), influencing experimental design and virus kinetics in mouse models.

These findings establish MAR1-5A3 as a powerful tool for:

  • Temporarily disabling type I IFN signaling in vivo without genetic knockouts.
  • Dissecting how type I IFN pathways shape immune responses to infection, vaccination, and tumor immunity.
  • Facilitating modeling of severe viral diseases and vaccine evaluation, especially for viruses poorly infectious in immunocompetent mice.

Most studies agree on these findings, although specific pathogenic outcomes and immunological consequences may vary depending on experimental context and viral factors.

References & Citations

1.) Beaver, Jacob T. et al. (2020) Human Vaccines & Immunotherapeutics 16:9, 2092-2108 Article Link
2.) Theofilopoulos, AN. et al. (2012) J Immunol. 189: 000–000. Article Link
3.) Oldstone, Michael B. A. et al. (2017) Proc Natl Acad Sci U S A. 114(14): 3708–3713. PubMed
4.) Schreiber, RD et al. (2015) PLoS One.10(5):e0128636PubMed
5.) Shin, Haina et al. (2018) J Virol. 92(7): e00038-18. PubMed
6.) Crack, Peter J. et al. (2016) eNeuro 10.1523/ENEURO.0128-15.2016 Article Link
7.) Sheehan, K. C. F. et al. (2006) JICR 26(11):804
8.) Dunn, G. P. et al. (2005) Nat. Immunol. 6(7):722
9.) Fenner, J. E. et al. (2006) Nat. Immunol. 7(1):33
10). Biron, C. A. et al. (2007) J Exp Med. 204(10): 2383
11.) Raju, S et al. (2019) Cell Reports. 29(9):2556–2564.e3 Journal Link
12.) Ortiz, A. et al. (2019) Cancer Cell 35(1):33-45.e6 Journal Link
13.) Case, J. et al. (2020) Cell Host & Microbe. 28(3):465–474.e4 Journal Link
14.) Hassan, A. et al. (2020) Cell. 183(1):169–184.e13 Journal Link
15.) Hassan, A. et al. (2020) Cell. 182(3):744–753.e4 Journal Link
16.) Hassan, A. et al. (2020) Cell. 182(3):901-918.e18 Journal Link
17.) Stine, R. et al. (2019) Cell Stem Cell. 25(6):830–845.e8 Journal Link
18.) White, J. et al. (2018) Cell 175(5):1198-1212.e12 Journal Link
19.) Jagger et al. (2017) Cell Host & Microbe. 22:366–376 Journal Link
20.) Richner, J. et al. (2017) Cell 170(2):273-283.e12 Journal Link
21.) Richner, J. et al. (2017) Cell 168(6):1114-1125.e10 Journal Link
22.) Best, S. et al. (2021) Cell Reports 37(4):109888 Journal Link
23.) Diamond, M. et al. (2021) Cell 184(17):Pages 4414-4429.e19 Journal Link
24.) Ahmed, H.et al. (2021) Cell Reports 36(4): 109452 Journal Link
25.) Lebratti, T.et al. (2021) eLife 10: e65762 Journal Link
26.) Gambino Jr., F.et al. (2021) Cell Reports 35(6): 109107 Journal Link
27.) Earnest, J. et al. (2021) Cell Reports 35(1): 108962 Journal Link
28.) Desai, P. et al. (2021) Cell 184(5):1214-1231.e16 Journal Link
29.) Jagger, B. et al. (2017) Cell Host Microbe 22(3):366-376.e3 Journal Link
30.) VanBlargan, L. et al. (2018) Cell Reports 25(12):10.1016 Journal Link
31.) Lim, J. et al. (2019) eLife 8(e44452):10.7554 Journal Link
B
Indirect Elisa Protocol
Flow Cytometry
in vivo Protocol
Immunoprecipitation Protocol
General Western Blot Protocol

Certificate of Analysis

- -
- -

Formats Available

- -
- -
Disclaimer AlertProducts are for research use only. Not for use in diagnostic or therapeutic procedures.