Anti-Mouse CD120a (TNFR1) [Clone 55R-170]

Clone 55R-170 is most commonly used in vivo in mice to block or neutralize the bioactivity of TNF Receptor I (CD120a/TNFRI), thereby inhibiting TNFRI-mediated signaling pathways. This application allows researchers to dissect the specific role of TNFRI in inflammatory, infectious, and autoimmune disease models, as well as in studies of TNF-induced pathology in vivo.

Key in vivo applications include:

• Neutralization of TNFRI signaling: 55R-170 is used to inhibit ligand-receptor interactions between TNF-α or lymphotoxin-α and TNFRI, which suppresses downstream signaling events such as inflammation, apoptosis, and cytokine release in various disease models.

• Investigating TNF-mediated pathology: The antibody is frequently applied in models of systemic inflammation (e.g., LPS-induced endotoxin shock), autoimmune diseases, and infection to evaluate the contribution of TNFRI signaling to disease severity, immune response, and pathology. For instance, administration of 55R-170 protected mice from lethal endotoxin shock and blocked protective immune responses against bacterial infections (e.g., Listeria monocytogenes), highlighting its capability to modulate in vivo immune responses through TNFRI blockade.

• Functional dissection of TNFRI vs. TNFRII: Because 55R-170 specifically targets the p55 (TNFRI) receptor (without cross-reactivity to p75/TNFRII), it is used to distinguish between the roles of the two TNF receptors in disease models, such as separating their involvement in skin necrosis, immune regulation, and inflammatory tissue injury.

• Control of TNF bioactivity in preclinical mouse models: Researchers use 55R-170 to modulate or neutralize TNF-dependent effects in vivo, making it a valuable tool for evaluating the impact of TNFRI blockade in the context of drug development for TNF-related diseases.

In summary, clone 55R-170 is a standard in vivo tool for selective TNFRI blockade, particularly in inflammation, infection, and TNF-driven disease studies in mouse models.

Other commonly used antibodies or proteins in the literature with 55R-170 (anti-mouse TNF receptor type I, TNFRI) include:

• Anti-mouse TNF receptor type II (TNFRII/p75) antibodies: Frequently used to distinguish or compare signaling roles between TNFRI (targeted by 55R-170) and TNFRII in functional experiments.
• Anti-TNF-α and anti-LT-α (lymphotoxin-α) antibodies: These are the principal ligands for TNFRI, and are often used for detection or neutralization in studies involving 55R-170.
• Anti-mouse CD120b (TNFRII) antibodies: Because CD120a and CD120b represent TNF receptor family members (TNFRI and TNFRII), studies often employ antibodies against both.
• 55R-286 antibody: Specifically cited as a commonly paired antibody in ELISA, where biotinylated 55R-170 is used as the detection antibody alongside purified 55R-286.

These antibodies are used to dissect TNF signaling, distinguish receptor-specific effects, or for biomarker detection in cytokine assays and flow cytometry. Additionally, antibodies targeting downstream signaling molecules or functionally related proteins, such as TRADD, TRAF2, or even regulatory proteins like BAG4/SODD (which interact with TNFR1), may occasionally be used in combination, depending on the experimental design, though specific clones for those targets are less frequently named in association with 55R-170.

The key findings from scientific literature citing clone 55R-170 center on its use as a monoclonal antibody for specifically blocking mouse TNFR1 (CD120a) signaling, which has provided significant insights into the roles of TNFR1 in inflammation, cell death, immune response, and disease models.

Essential findings include:

• Specific antagonist of TNFR1: Clone 55R-170 binds and antagonizes mouse TNFR1, effectively blocking receptor signaling both in vitro and in vivo, allowing researchers to dissect TNFR1-specific effects apart from TNFR2.
• Dissection of TNFR1 function: Its use has helped define distinct and non-redundant roles of TNFR1 versus TNFR2 in pathways such as apoptosis (cell death), NF-κB activation, inflammation, and disease progression (including tumor growth and autoimmune disease).
• In vivo disease model studies: Blocking TNFR1 with 55R-170 has been shown to:
  • Reduce inflammation and pathologic immune responses, helping to clarify the TNFR1-dependent steps in cytokine storm and chronic inflammatory diseases.
  • Enhance antitumor immune response in cancer models by preventing TNFR1-mediated immunosuppression, leading to improved T cell activity and slower tumor growth.
  • Reveal that genetic or antibody-mediated TNFR1 blockade can synergize with other therapies, such as immune checkpoint inhibitors (e.g., anti-PD-1), overcoming resistance in solid tumors.
• Experimental versatility: Clone 55R-170 is validated for varied applications (e.g., flow cytometry, ELISA, immunoprecipitation, Western blot, and animal studies), making it a widely used tool in mouse immunology research.
• Mechanistic and therapeutic insights: Its use has driven the generation of new therapeutic hypotheses targeting TNFR1-dependent mechanisms, relevant for translating findings to human diseases that involve TNF signaling pathways.

Reference highlights:

• Dana et al. (Arch Ophthalmol. 2000) and Pasparakis et al. (Nat Immunol. 2008) used 55R-170 to study inflammation and immune cell activation in eye and systemic models, respectively.
• Donner et al. (J Immunol. 2008) and follow-up studies characterized TNFR1’s apoptotic domain and its requirement for apoptosis induction and NF-κB signaling.
• Tumor studies demonstrated that TNFR1 blockade can slow pancreatic cancer growth by modulating intratumor T cell activation.
• Combination therapy studies suggest TNFR1 blockade overcomes resistance to anti-PD-1 checkpoint blockade in cancer.

Summary:
Clone 55R-170 is a rigorously validated research tool for selectively blocking TNFR1 signaling in mice, enabling scientists to clarify TNFR1’s roles in inflammation, apoptosis, and cancer immunity, and laying groundwork for translational therapeutic interventions.

Based on available information, there are no well-established standardized dosing regimens for clone 55R-170 (anti-mouse CD120a/TNFR1) that vary systematically across different mouse models. The dosing protocols for this antibody must be adapted empirically for individual studies rather than following model-specific guidelines.

Limited Dosing Information Available

No clear indications exist that dosing for 55R-170 changes meaningfully based on specific mouse strains, disease states, or experimental models. The antibody has been characterized primarily for its neutralizing activity against TNF receptor I, with in vitro data showing that 25 µg/mL can inhibit by 50% the biological effects of 1 ng/mL mouse TNF alpha in cytotoxicity assays. However, this in vitro characterization does not translate directly to standardized in vivo dosing schedules.

General Dosing Considerations

For similar neutralizing antibodies to cytokine receptors in mice, typical starting doses in published protocols range from 100–250 µg per mouse. This provides a reasonable starting point for researchers designing experiments with 55R-170, though optimization for specific experimental contexts remains necessary. The antibody has been formulated for in vivo use with low endotoxin levels (<0.001 ng/µg) and is available in functional grade preparations suitable for animal studies.

Empirical Approach Required

Since protocols must be adapted empirically for individual studies, researchers need to conduct pilot experiments to determine optimal dosing for their specific application, whether studying inflammation, autoimmune disease models, or other TNF-mediated processes. Testing in multiple models and mouse strains with clinically relevant treatment regimens is prudent for translational research.