Anti-Mouse CTLA-4 (CD152) [Clone UC10-4F10-11] — Purified in vivo GOLD™ Functional Grade

The clone UC10-4F10-11 is widely used in in vivo mouse studies as an Armenian hamster IgG monoclonal antibody that specifically targets mouse CTLA-4 (CD152) and serves as a potent neutralizing antibody for CTLA-4.

In vivo, UC10-4F10-11:

• Neutralizes CTLA-4 activity, thereby modulating T cell responses.
• Blocks CTLA-4 binding to its ligands (B7 co-receptors), which enables CD28-mediated co-stimulation of T cells, enhancing T cell activation.
• Is used for research on T cell activation, immune checkpoint blockade, and tumor immunology in mouse models.
• Is validated and commonly used in preclinical immune-oncology studies, especially when exploring mechanisms of immune checkpoint blockade therapies.
• Can also be used for flow cytometry and Western blotting to detect murine CTLA-4 expression.

According to manufacturers and published literature, this antibody is offered in low endotoxin preparations for in vivo applications, and recommended isotype controls are available to ensure specificity in animal studies. Researchers typically select the UC10-4F10-11 clone for its documented ability to neutralize CTLA-4 both in vitro and in vivo, thereby facilitating enhanced T cell immune responses in experimental mouse models.

Other commonly used antibodies or proteins with UC10-4F10-11 in the literature include additional anti-CTLA-4 antibody clones, isotype controls, and protein ligands relevant to T-cell co-stimulation and regulation.

Key examples:

• Other anti-CTLA-4 clones: The literature often compares or co-utilizes UC10-4F10-11 with 9H10 (Syrian hamster IgG) and 9D9 (mouse IgG2b), each featuring distinct host species and functional characteristics. 9H10 is particularly notable for stronger regulatory T cell (Treg) depletion in tumor models compared to 9D9, as well as robust CTLA-4 neutralization both in vitro and in vivo.
• Isotype controls: For experimental rigor, the Armenian Hamster IgG Isotype Control is routinely paired with UC10-4F10-11 in vivo to rule out non-specific effects; similar isotype controls exist for the other clones in their host species, such as mouse or Syrian hamster.
• Ligands and co-receptors: UC10-4F10-11 influences interactions with B7 co-receptors (CD80/CD86) and CD28, proteins involved in T-cell activation. While not antibodies, these are essential molecular players when studying or manipulating CTLA-4 function, especially in assays measuring T cell co-stimulation or regulatory suppression.

Experimental approaches frequently involve the simultaneous detection of CTLA-4 (CD152) or the use of Western blot or flow cytometry with UC10-4F10-11, supported by these controls and other clones for comparison of specificity, depletion efficacy, and cross-reactivity.

In summary, commonly paired or compared reagents include:

• Anti-CTLA-4 clones: 9H10, 9D9
• Isotype controls: Armenian hamster IgG (for UC10-4F10-11), mouse IgG2b (for 9D9), Syrian hamster IgG (for 9H10)
• Protein ligands and co-receptors: B7 family (CD80/CD86), CD28

These combinations enable precise study of T cell regulation, co-stimulation, and tumor immunology.

Key Findings from Clone UC10-4F10-11 Citations

Clone UC10-4F10-11 is an Armenian hamster IgG monoclonal antibody used to target mouse CTLA-4 (CD152), primarily in preclinical research. Below is a summary of the most significant scientific findings and applications associated with this clone, based on the available literature:

Functional and Mechanistic Insights

• CTLA-4 Blockade: UC10-4F10-11 functions by blocking CTLA-4 engagement with its ligands, the B7 co-receptors B7-1 (CD80) and B7-2 (CD86), thereby preventing the inhibitory signal mediated by CTLA-4 and allowing co-stimulation via CD28 activation. This blockade promotes T cell activation and proliferation in both in vitro and in vivo contexts.
• Cell Type Expression: The target CD152 (CTLA-4) is expressed on T lymphocytes 2–3 days after activation via the T cell receptor, and UC10-4F10-11 specifically recognizes this expressed form.
• Immunodepletion: While its main action is functional blockade of CTLA-4 signaling, UC10-4F10-11 may also partially deplete regulatory T cells (Tregs) within tumors, although this effect is less pronounced compared to other clones such as 9H10.

Immunological Effects in Animal Models

• Th2 Skewing: Administration of UC10-4F10-11 during the priming phase of the immune response in mice drives the generation of IL-10- and IL-4-producing T cells, leading to impaired memory Th1 (IFN?-producing) responses. This suggests a shift toward a Th2-type cytokine profile and a dampening of Th1-mediated immunity.
• Protection in Colitis Model: In a TNBS-induced colitis model, UC10-4F10-11 injection conferred significant protection against disease, likely due to enhanced IL-10 production and suppression of pathogenic Th1 memory responses.
• ICOS+ Treg Induction: The antibody treatment increases the frequency of ICOS-high, IL-10-producing regulatory T cells, which may mediate some of the protective effects in autoimmune inflammation.
• STAT6 Dependency: The development of ICOS-high, IL-10-producing cells in response to UC10-4F10-11 is impaired in STAT6-deficient mice, indicating that this pathway is partially dependent on STAT6, a transcription factor associated with Th2 differentiation.

Technical and Application Notes

• Detection Methods: UC10-4F10-11 is effective for Western blot detection of murine CTLA-4 and is also suitable for flow cytometry.
• Antibody Production: The clone is purified by multi-step affinity chromatography to ensure low endotoxin levels (<1 EU/mg) and minimal protein aggregation (<5%), making it suitable for in vivo studies.
• Availability: It is commercially available from suppliers such as Bio X Cell and ichorbio, both in purified and low-endotoxin formats.
• Comparative Efficacy: Among commonly used anti-CTLA-4 clones, UC10-4F10-11 is noted for its neutralizing capacity but may have less potent Treg-depleting activity compared with clone 9H10.

Summary Table: Key Attributes of UC10-4F10-11

Conclusion

Clone UC10-4F10-11 is a well-characterized tool for studying CTLA-4 function in mice. Its key scientific findings include potent blockade of CTLA-4-mediated inhibition, induction of IL-10-producing regulatory T cells, skewing of immune responses toward a Th2 phenotype, and protective effects in models of autoimmunity—highlighting its utility for dissecting mechanisms of immune regulation and tolerance.

The dosing regimen for clone UC10-4F10-11 (anti-mouse CTLA-4) varies depending on the mouse model and experimental goals, but the most commonly used in vivo doses range from 50–250?µg per mouse, typically delivered via intraperitoneal injection. Specific schedules and amounts may differ based on the study design, disease model, or targeted immune response.

Supporting details from published studies and reagent guides:

• General recommended dose: Manufacturers advise 50–250?µg/mouse for in vivo studies with this clone; researchers should optimize the dose for their particular model.
• Immunization models: In T cell priming studies, 100?µg/mouse UC10-4F10-11 was administered on days 3, 4, and 5 following antigen exposure.
• Tumor rejection models: One publication reports UC10-4F10-11 given at three single time points (specific doses not detailed in the abstract, but similar checkpoint antibodies typically use 100–250?µg/mouse per injection as per standard mouse oncology protocols).
• General checkpoint blockade paradigms: Other anti-CTLA-4 clones (e.g., 9H10, 9D9) are frequently dosed at 100–250?µg/mouse every 3 days for cancer immunotherapy or immune activation studies, suggesting this is a typical regimen for UC10-4F10-11 as well.

Route of administration:

• The standard route is intraperitoneal injection in most published studies and reagent guidelines.

Variation across models:

• The exact dosing schedule (frequency, timing) can be adapted based on:
  • Purpose (e.g., immune priming, cancer immunotherapy, autoimmunity)
  • Mouse strain or disease model (e.g., syngeneic tumor challenge, antigen-induced inflammation)
  • Combination therapies (UC10-4F10-11 may be used with anti-PD-1/PD-L1 antibodies; each has its own optimal schedule)

Optimization:

• Investigators are encouraged to determine the optimal dosing regimen for their specific application, as immune response and toxicity thresholds may vary between models.

Summary table:

Key points:

• Dose range: 50–250?µg per mouse, with 100?µg common for immunology studies.
• Schedule: Every 3 days or targeted to specific time points, often multiple injections for induction and maintenance.
• Route: Intraperitoneal recommended.
• Specific regimen should be optimized for the experimental model and validated by pilot studies.

No evidence from the search results indicates large differences in standard dosing between major mouse models; instead, schedule and frequency are tailored to the research context.