Anti-Mouse/Human IL-5 – Purified in vivo GOLD™ Functional Grade

Clone TRFK5 is commonly used in vivo in mice to neutralize interleukin-5 (IL-5) bioactivity and deplete eosinophils, allowing researchers to study the role of IL-5 in immune responses, particularly in models of allergy, asthma, and tumor progression.

Key in vivo applications include:

• Neutralization of IL-5 bioactivity: TRFK5 binds to IL-5 and blocks its biological function, preventing its interaction with receptors on target cells.
• Eosinophil depletion: Because IL-5 is crucial for the differentiation, proliferation, and survival of eosinophils, in vivo administration of TRFK5 reduces eosinophil counts in blood and tissues.
• Functional studies in disease models: TRFK5 is used to dissect the role of IL-5 and eosinophils in mouse models of IL-5–driven diseases, such as allergic airway inflammation (e.g., asthma), tumor-associated immune responses (such as malignant pleural effusion), and other eosinophilic disorders.

Supporting details:

• In one cancer model, TRFK5 administration in mice with tumor-induced malignant pleural effusion resulted in significantly lower numbers of eosinophils in effusion fluid and tumor tissue, as well as reduced myeloid suppressor cell recruitment compared to controls.
• In asthma and allergy research, in vivo TRFK5 treatment is a standard approach for IL-5 blockade, helping define the cytokine’s key role in eosinophilia and airway inflammation.
• The antibody is also utilized for benchmarking mutant or knockout models where IL-5 or its receptor is absent, providing complementary pharmacological inhibition of the pathway.

Other reported uses:

• Though TRFK5 is widely validated for neutralization and depletion in vivo, it is also standard for in vitro applications including ELISA, ELISPOT, flow cytometry, and immunohistochemistry, but these are not in vivo uses.

In summary, in vivo applications of TRFK5 in mice focus on IL-5 neutralization and eosinophil depletion to elucidate disease mechanisms dependent on these pathways, with particular relevance to allergy, asthma, and certain cancer models.

Commonly used antibodies or proteins paired with TRFK5 in the literature typically target IL-5, with other antibodies serving as detection or capture partners depending on species and application. The most frequently referenced partners and related reagents include:

• TRFK4 antibody: Often employed as the detection antibody in mouse IL-5 ELISA/ELISPOT assays when TRFK5 is used for capture.
• JES1-5A10 antibody: Utilized as the detection antibody for human IL-5 in ELISA protocols, with TRFK5 serving as the capture antibody.
• Recombinant IL-5 proteins: Both mouse and human recombinant IL-5 are commonly used standards in bioassays and ELISA for calibration and positive controls.
• Other applications: TRFK5 is also frequently used in neutralization assays and flow cytometry—for the latter, it may be conjugated to fluorochromes or used alongside different detection antibodies or markers to identify IL-5–producing cells.
• Related proteins or markers in immunophenotyping: Studies may also involve other immune markers such as CD4 (T cells) and immunoglobulins (e.g., IgE, IgG) when examining immune responses in vivo, especially in pulmonary inflammation models.
• Additional clones: BAM6051 is noted as a detection antibody in certain immunoassays with TRFK5 as the capture.

In summary, the most common pairings for TRFK5 in published protocols and commercial kits involve TRFK4 (mouse), JES1-5A10 (human), and standard recombinant IL-5 proteins. These partners are selected based on the target species and the specific immunoassay format such as ELISA, ELISPOT, or flow cytometry.

Key findings from scientific literature citing clone TRFK5—an anti-interleukin-5 (IL-5) monoclonal antibody—consistently demonstrate its utility in neutralizing IL-5 bioactivity, leading to marked reductions in eosinophilic activity and associated pathological effects.

Principal findings include:

• Eosinophil Depletion: TRFK5 effectively depletes eosinophils in various tissues and settings. For instance, treatment with TRFK5 in murine models significantly reduced eosinophil numbers in cutaneous wounds and pleural tumors, confirming its specificity and efficacy in vivo.

• Therapeutic Effects in Disease Models:

  • In models of malignant pleural effusion (MPE), TRFK5 administration both prevented and reduced established MPE formation and suppressed intrapleural tumor growth.
  • In wound healing studies, TRFK5-treated animals exhibited accelerated wound closure (re-epithelialization) compared to controls, indicating that eosinophils—whose infiltration TRFK5 abrogates—may negatively affect wound healing.

• Mechanisms of Action:

  • TRFK5 selectively neutralizes both natural and recombinant IL-5, impacting eosinophil recruitment, survival, and activation.
  • These effects confirm the critical role of IL-5 in promoting eosinophilic responses and implicate TRFK5 as a tool for mechanistic dissection of IL-5-mediated processes.

• Downstream Effects:

  • Reduction in myeloid-derived suppressor cells (MDSCs): In cancer models, TRFK5 treatment not only reduced eosinophils but also decreased the recruitment of MDSCs to tumor microenvironments, potentially mitigating tumor-promoting inflammation.
  • In pleural tumors and MPE, VEGF, TNF-α, MCP-1, and IL-6 levels were unchanged by TRFK5, signifying the selectivity of IL-5 blockade.

• Neutralization in Multiple Applications: TRFK5 is widely used for in vivo IL-5 neutralization and eosinophil depletion, both in research and preclinical therapeutic contexts, further validating its specificity and reproducibility.

Summary Table: Primary Actions and Outcomes of TRFK5 Use

General Context:
Because TRFK5 neutralizes IL-5 activity, its primary experimental value lies in studies of allergic disease, asthma, parasitic infection, wound repair, and cancer, wherever eosinophilic inflammation is implicated.

These findings indicate that TRFK5 citations most often highlight its ability to reduce IL-5-mediated eosinophil recruitment and activity, thereby modulating disease outcomes and serving as a valuable investigative and preclinical tool.

Dosing regimens of clone TRFK5 in mouse models typically vary by the experimental context, treatment schedule, disease model, and intended degree of IL-5 neutralization, but most studies use intraperitoneal (i.p.) injections in the range of 1 mg/kg per dose, with dosing frequency tailored to the timeline of the immune response or therapeutic intervention.

Key dosing information and variations across studies:

• General Standard Regimen:
  The most common single-dose regimen for TRFK5 in vivo is 1 mg/kg administered intraperitoneally (i.p.), though this can be adjusted based on the specific experimental requirements. Some protocols administer a single dose 1 day before the main experimental treatment, especially in cancer immunotherapy or depletion studies.

• Alternate Dosing Schedules:

  • Some studies use multiple doses of 0.3 mg/mouse given every 3 days, amounting to a total dose of 50 mg/kg over the course of the experiment.
  • Dosing frequency often matches the anticipated duration of IL-5-mediated effects. For example, in combination immunotherapy in cancer, TRFK5 is typically administered 1 day prior to therapy and repeated before each round of treatment.

• Variability by Disease Model:

  • In allergic airway or asthma models, the 1 mg/kg i.p. dose every few days is common, potentially repeated over several days or weeks.
  • In tumor models (e.g., lung cancer, pleural effusion), similar regimens are applied, with reported reductions in eosinophil and myeloid suppressor cell numbers upon TRFK5 administration.

• Adjustment Factors:
  The exact regimen may be adjusted for:

  • Antibody half-life in the chosen mouse model and experimental conditions,
  • Disease pathophysiology (e.g., acute vs. chronic inflammation),
  • Whether the aim is full neutralization or partial IL-5 blockade.

Summary Table: Common TRFK5 Dosing Regimens

• Important Note:
  The optimal dosing interval and amount is influenced by the mouse strain, specific disease model, and experimental goals, and should be titrated for adequate IL-5 neutralization. Always consult the primary literature for your disease context and verify requirements with the antibody supplier.

• Regulatory caveat:
  TRFK5 regimens are for research use only and may require validation for your specific application.

If you have a specific disease model in mind, further detail can be provided based on published protocols for that context.