GL3 Antibody
Description
Introduction to GL3 Antibody
The GL3 antibody is a monoclonal antibody targeting the gamma delta (γδ) T-cell receptor (TCR), a specialized receptor expressed on γδ T cells. These cells are a subset of T lymphocytes involved in bridging innate and adaptive immunity, found in epithelial tissues, lymphoid organs, and mucosal surfaces . GL3 is widely used in immunology research to identify, isolate, and modulate γδ T cells in vitro and in vivo .
Mechanism of Action
The GL3 antibody specifically binds to the γδ TCR complex without cross-reacting with αβ TCR . Key features include:
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Epitope Recognition: Targets a conserved epitope on the γδ TCR, enabling detection across diverse tissues (e.g., thymus, intestine, lymphoid organs) .
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Functional Modulation: Induces TCR internalization upon binding, rendering γδ T cells "invisible" to detection without depleting them .
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Cross-Reactivity: Competes with other anti-γδ TCR antibodies (e.g., UC7-13D5) for binding, suggesting overlapping epitopes .
Research Applications
GL3 is validated for multiple experimental workflows:
Comparative Analysis with VP-16 in Anticancer Research
GL3 is distinct from the chemotherapeutic agent GL3 (4β-anilino-4′-O-demethyl-4-desoxypodophyllotoxin), a VP-16 derivative. Key differences:
Note: The chemotherapeutic GL3 is unrelated to the antibody but shares the same abbreviated name .
In Vivo Effects and Modulatory Role
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TCR Internalization: GL3 treatment causes γδ TCR internalization, reducing surface expression while preserving cell viability .
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Immune Crosstalk: Modulated γδ T cells indirectly enhance αβ T-cell proliferation and cytokine production (e.g., IL-2) .
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Disease Models: Used to study γδ T-cell roles in infections, autoimmunity, and cancer .
Key Research Findings
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Anticancer Activity (Compound GL3): Demonstrates 10-fold higher cytotoxicity than VP-16 in lung and oral cancer cells (IC50: 0.82 µM vs. 4.18 µM) .
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Immunoregulation: GL3-treated γδ T cells suppress graft-versus-host disease (GVHD) and enhance bacterial clearance .
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Technical Caveats: GL3 does not deplete γδ T cells in vivo, necessitating complementary methods for functional studies .
Product Specs
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
- At1g01380 protein can inhibit the interaction between the positive trichome regulators GL1 and GL3, potentially limiting trichome initiation through this inhibition. [GL3] PMID: 15584952
- A contradictory GLABRA3 allele contributes to defining gene interactions that control trichome development in Arabidopsis. PMID: 14561633
- Data suggest that GLABRA3 (GL3)-mediated gene expression exhibits tissue specificity. PMID: 28216162
- GL3 influences the expression of UPL3. PMID: 23373825
- GL3::SlGL3 transformation did not exhibit any obvious effect on trichome or non-hair cell differentiation. This finding suggests that tomato and Arabidopsis utilize partially similar transcription factors for epidermal cell differentiation. PMID: 23326563
- A novel interaction between mutant alleles of GLABRA3 and SIAMESE, both essential for differentiation, is reported. PMID: 17764505
- The role of GL3 in the initiation of trichomes from pluripotent epidermal cells in Arabidopsis is described. PMID: 17885086
- Data indicate that GL3 associates with TRANSPARENT TESTA GLABRA1 in vivo, forming a complex. PMID: 18434419
- The role of GL3 in Arabidopsis trichome formation is investigated. PMID: 18547143
- GL3 is identified as a key transcription factor involved in wound-induced trichome formation, acting downstream of jasmonic acid signaling in Arabidopsis. PMID: 19234066
- Anthocyanins accumulate in both wild type and egl3, but not in gl3 loss-of-function mutants when depleted of nitrogen. PMID: 19621239
- GL3 and EGL3 participate in an intercellular regulatory circuit that controls cell patterning in the Arabidopsis root epidermis. [GL3] PMID: 15590742
Q&A
Here’s a structured FAQ for researchers working with the GL3 antibody, organized by scientific complexity and methodological focus:
Advanced Research Questions
Case Example:
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Issue: Discrepancies in cytokine profiles (IFN-γ vs. IL-17) in infection models.
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Solution:
Table 2: GL3 vs. Alternative Clones
| Clone | Target Epitope | Functional Use Case | Limitation | Source |
|---|---|---|---|---|
| GL3 | Pan-γδ TCR | Depletion, IHC, flow cytometry | Does not block TCR signaling | |
| UC7-13D5 | Vγ2 chain | Subset-specific studies | Limited to human cells |
Approach:
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Antigen Binding: Co-stain with Cy3-OVA (2 µg/mL) and HA-dextramer (1.35 µM) at 37°C for 1 hr .
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Functional Assays:
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Controls: Include αβ T cells and γδ TCR KO mice to exclude bystander activation .
Solutions:
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Fixation: Use acetone-frozen sections for IHC; avoid paraformaldehyde-induced epitope masking .
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Antigen Retrieval: Pre-treat intestinal epithelium samples with collagenase IV (1 mg/mL, 30 min) .
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Validation: Compare with RNAscope for TCRγδ mRNA in GL3-negative populations .
Key Research Findings
Polyspecific γδ T Cell Dynamics
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Frequency: 1.5–30% of murine γδ T cells exhibit Cy3/HA polyspecificity .
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Functional Role: Polyspecific cells show elevated CD44 and reduced CD62L, indicating antigen-experienced phenotypes .
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Human Relevance: Similar polyspecificity observed in human PBMCs, with variable frequencies (2–80%) linked to immune history .
