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.
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
The anti-mouse γ/δ T-cell receptor antibody reacts with all mouse TCR γ/δ heterodimers.
Background
The T cell receptor or TCR is a molecule found on the surface of T lymphocytes that is responsible for recognizing antigens bound to major histocompatibility complex (MHC) molecules. It is a heterodimer consisting of an α and β chain in 95% of T cells, while 5% of T cells have TCRs consisting of γ and δ chains. Engagement of the TCR with antigen and MHC results in activation of its T lymphocyte through a series of biochemical events mediated by associated enzymes, co-receptors and specialized accessory molecules.
Antigen Distribution
γδ TCR expression is observed on a subset of cells in the thymus, intestinal epithelium, skin, liver, peripheral lymphoid tissues, and peritoneum. The γδ TCR is involved in the antigen recognition of some bacterial or tumor-associated antigens presented by MHC class I.
Ligand/Receptor
Some bacterial or tumor antigens bound MHC class I
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The most common in vivo application of clone UC7-13D5 in mice is the depletion of γδ (gamma delta) T cells to study their functional roles in various immune responses. This is achieved by administering the antibody to selectively target and remove γδ T cells from circulation.
Key details and context:
Depletion studies: Researchers routinely inject UC7-13D5 into mice to deplete γδ T cells, allowing experiments that probe the function of these cells in infection, cancer, autoimmune disease, and immune regulation.
Mechanism and considerations: Although depletion is the most reported use, some studies indicate that the antibody may not always lead to true cell depletion. Instead, it may cause internalization or downregulation of the γδ TCR, making the cells undetectable by standard detection methods, even though the cells are still present. This is a crucial consideration in interpreting experimental outcomes.
Alternative effects: There is evidence suggesting UC7-13D5 can also functionally block TCR signaling in vivo without complete cellular removal, depending on the experimental system and assay readout.
Other applications: Outside in vivo depletion, UC7-13D5 is widely used in flow cytometric phenotyping, functional blocking assays, immunoprecipitation, and sometimes for in vitro activation of γδ T cells.
Summary table: Common in vivo applications of UC7-13D5 in mice
Application
Details
Key Considerations
Depletion of γδ T cells
Removal of γδ T cells from circulation to analyze their role in immunity
True depletion vs. TCR masking/internalization
Functional TCR blockade
Blocks γδ TCR-mediated signaling in vivo
May not remove cells, just inactivate their signaling
Phenotypic marker (less common in vivo)
In combination with other antibodies for tracking γδ T cells by flow cytometry
Useful for cell monitoring, not for depletion
Researchers should validate γδ T cell depletion in their particular system with appropriate controls and consider that undetectable cells may remain functionally silent rather than fully eliminated.
In the literature, UC7-13D5 (an anti-mouse TCR γ/δ antibody) is most commonly used with the following antibodies and proteins:
Anti-CD3: Used to identify T cells and discriminate total T cells from γδ T cells when staining for flow cytometry.
Anti-CD4: Used to distinguish helper T cells and help differentiate between γδ T cells (which are typically CD4–, CD8– or double negative) and other lymphocyte subsets.
Anti-CD8: Used alongside CD4 for further subset discrimination among T cells.
UC7-13D5 is often part of a panel that includes:
Anti-TCRβ: To compare γδ and αβ TCR T cells (e.g., using clone H57-597).
Anti-Vγ4: To identify specific γδ T cell subsets (e.g., using clone UC3-10A6).
Anti-TCRγδ (other clones): Such as GL3 or GL4, for cross-validation or comparative studies.
Activation Markers: Sometimes used with antibodies against early or late activation markers (e.g., CD69, CD25) as needed for specific functional studies (this is a common but less specifically cited practice).
Context and Supporting Use:
These combinations allow researchers to distinguish γδ T cells from αβ T cells, sort lymphocyte populations, and further define subsets during flow cytometry or immunohistochemistry.
When studying cell function, costimulation, or depletion experiments, anti-CD3, CD4, CD8, and related markers help define the immunological context of γδ T cells.
References to Illustrative Use:
A frequently referenced panel for flow cytometry included anti-CD4 (clone RM4-5), anti-CD8α (clone 53-6.7), anti-TCRγδ (GL3, GL4, UC7-13D5), anti-Vγ4 (UC3-10A6), and anti-TCRβ (H57-597).
Some studies simultaneously compare GL3 and UC7-13D5 against each other or use both to confirm findings about γδ T cell populations.
These markers are considered the standard for γδ T cell research involving UC7-13D5 and are central to phenotypic and functional studies of T cell subsets.
Key Findings from Scientific Literature on Clone UC7-13D5
Mechanism of Action In Vivo
TCR Internalization, Not Depletion: Multiple studies demonstrate that in vivo administration of the UC7-13D5 monoclonal antibody does not deplete γδ T cells, but instead induces internalization of the γδ TCR, rendering these cells "invisible" to standard detection methods such as flow cytometry. This was conclusively shown using reporter mice where γδ T cells could still be detected via intrinsic fluorescence despite antibody treatment.
Functional Blockade: Some reports suggest that UC7-13D5 may functionally block γδ TCR signaling rather than causing cell death. This is important for interpreting studies where "depletion" protocols are used, as the cells may remain present and potentially functional, but undetectable by conventional means.
Cross-Competition with Other Clones: UC7-13D5 and another commonly used antibody, GL3, partially compete for the same epitope on the γδ TCR, and both exhibit similar effects in vivo.
In Vitro Effects
T Cell Activation: Plate-bound UC7-13D5 can activate γδ TCR-bearing cells in vitro, indicating that the antibody can deliver stimulatory signals under certain conditions. This activation property is distinct from its effects in vivo, where internalization predominates.
Specificity: UC7-13D5 is highly specific for the mouse γδ TCR heterodimer and does not react with αβ TCR-expressing T cells.
Applications and Caveats
Experimental Use: UC7-13D5 is widely used in flow cytometry, immunoprecipitation, costimulation, and (purported) depletion assays. However, its primary effect in vivo is TCR downregulation, not true depletion.
Caution in Interpretation: The literature emphasizes that results from γδ T cell "depletion" experiments using UC7-13D5 (and similar antibodies) must be interpreted with caution, as the cells may persist in a functionally altered state.
Utility in Genetic Models: When true depletion is required, genetic models such as TCRδ chain knockout mice are recommended, as antibody-based approaches may not achieve actual cell loss.
Summary Table: Key Effects of UC7-13D5
Context
Effect
Evidence/Implication
In vivo
TCR internalization ("invisible" cells)
Cells remain present but undetectable
In vitro
Activation of γδ T cells
Plate-bound antibody stimulates TCR signaling
Specificity
Binds mouse γδ TCR, not αβ TCR
Useful for selectively targeting γδ T cells
Depletion
Not effective
Use genetic models for true depletion
Conclusion
The clone UC7-13D5 is a valuable tool for studying mouse γδ T cells, particularly for detection and in vitro stimulation. However, its in vivo use does not result in true depletion; instead, it causes TCR internalization, making γδ T cells undetectable by standard methods while potentially leaving them functionally intact. These findings highlight the need for careful experimental design and interpretation when using UC7-13D5 in vivo, and suggest that genetic models may be preferable for studies requiring actual γδ T cell ablation.
Dosing regimens for clone UC7-13D5 in mouse models are not standardized, but typically range from 100–250 µg per mouse per administration, with the exact dose and schedule selected based on the experimental goal, mouse strain, tissue, and specific protocol. Primary applications include in vivo depletion, activation, or functional blocking of γδ T cells.
Key factors influencing dosing regimens:
Experimental objective:
Depletion (in vivo): Typical doses reported are 100–250 µg per mouse via intraperitoneal injection. For example, a common protocol uses 0.2 mg (~200 µg) per mouse to deplete γδ T cells effectively. Some sources recommend a single dose, although repeated dosing on consecutive days is sometimes used for sustained depletion or depending on experiment length.
Functional blocking or receptor downregulation: Although UC7-13D5 is frequently cited for cell depletion, at least one study reports that the antibody may instead cause TCR downregulation—making cells undetectable by flow cytometry, but not actually depleting them in vivo. In such contexts, dosing regimens may mirror those for depletion but with careful monitoring for effective blockade versus actual cell loss.
Activation (in vitro): Plate-bound UC7-13D5 is used to activate γδ T cells, but these protocols are distinct from in vivo dosing and typically involve much lower concentrations.
Mouse model details:
Strain, age, tissue of interest, and disease or challenge model can all influence antibody requirements.
For example, in an MHC-mismatched graft-versus-host-disease (GVHD) model, UC7-13D5 was used to deplete IL-7R+ T cells—though specific dosing details should be cross-checked against original studies for that application.
Noteworthy protocol variations and limitations:
Verification of depletion: Some reports caution that UC7-13D5 does not necessarily cause physical depletion, instead masking or downregulating γδ TCR expression. Thus, functional studies should confirm actual cell loss by combining antibody treatment with alternative detection strategies.
Dose schedule: Most commonly, a single or limited series of intraperitoneal injections are used (e.g., once before or at the start of challenge, with or without repeat administration).
Controls: Isotype control antibodies are always recommended to distinguish specific effects from nonspecific immunoglobulin action.
Summary Table: Dose and Variation by Application
Application
Typical Dose
Frequency
Notes
In vivo depletion
100–250 µg/mouse
Single or repeated
Must verify actual depletion, not just downregulation
In vivo blocking/downregulation
100–250 µg/mouse
Single or repeated
May mask cells, not deplete—verify strategy
In vitro activation
Lower, variable
N/A
Plate-bound application—dose much lower than in vivo
In conclusion, dosing of UC7-13D5 in mouse models requires tailoring to the experimental aim and careful validation for actual cell depletion, with 100–250 µg/mouse being a typical range for in vivo use. Standardized protocols are lacking, so referencing published experiments most similar to your study design is strongly recommended.
References & Citations
1.) Bluestone, J. A et al. (1991) Immunol. Rev.120:5-33 Journal Link
2.) Hiromatsu K et al. (1992) J. Exp. Med.175 (1):49-56 Journal Link
3.) van der Heyde HC et al. (1995) J. Immunol.154 (8): 3985-3990 Journal Link
4.) Pollinger B et al. (2011) J. Immunol.186 (4):2602-12 Journal Link