Anti-Mouse TIGIT [Clone 1G9] — Purified in vivo PLATINUM™ Functional Grade

In Vivo Applications of Clone 1G9 in Mice

Clone 1G9 is a mouse monoclonal antibody (IgG1, κ) that specifically recognizes mouse TIGIT (T cell immunoreceptor with Ig and ITIM domains). Its in vivo use is primarily as an agonistic antibody to modulate immune responses mediated by TIGIT, an inhibitory immune checkpoint receptor expressed on T cells, including regulatory T cells (Tregs) and subsets of activated and memory T cells.

Key In Vivo Applications

• Suppression of T Cell-Driven Inflammation: Clone 1G9 is used in vivo to suppress T cell-driven inflammation in mice. By delivering agonistic signals through TIGIT, it reduces T cell expansion and the production of pro-inflammatory cytokines, thereby attenuating autoimmune and inflammatory responses. This makes it a valuable tool for studying the role of TIGIT in autoimmune diseases and immune regulation.
• Investigation of Immune Checkpoint Modulation: As an immune checkpoint molecule, TIGIT negatively regulates T cell and NK cell activation. In vivo administration of 1G9 allows researchers to probe the consequences of TIGIT pathway engagement, including effects on immune tolerance, cytokine profiles, and the balance between immune activation and suppression.
• Blockade of TIGIT/CD155 Interaction: In vitro, 1G9 fully blocks the binding of TIGIT to its high-affinity ligand CD155. While in vivo experiments confirm that 1G9 does not deplete TIGIT+ cells under steady-state conditions, its primary effect is functional blockade of the TIGIT pathway rather than cell depletion.
• Flow Cytometry and Phenotyping: Although primarily an in vivo tool, 1G9 is also used for flow cytometry to identify and characterize TIGIT-expressing cell populations in mice. However, its most distinctive utility is in modulating immune responses in living animals.

Experimental Impact

• Reduced T Cell Expansion: In vivo, 1G9 treatment leads to decreased T cell proliferation, highlighting TIGIT’s role in restraining excessive immune activation.
• Diminished Pro-Inflammatory Cytokine Production: The antibody reduces the secretion of pro-inflammatory cytokines, consistent with TIGIT’s immunosuppressive function.
• No Cell Depletion: Unlike some therapeutic antibodies, 1G9 does not cause depletion of TIGIT-expressing cells, allowing researchers to study the functional consequences of pathway engagement without confounding effects of cell loss.

Summary Table

Conclusion

Clone 1G9 is principally employed in mice to agonize TIGIT signaling in vivo, thereby suppressing T cell-driven inflammation and modulating immune checkpoint activity without depleting TIGIT+ cells. This makes it a critical reagent for investigating the immunoregulatory functions of TIGIT in autoimmune, inflammatory, and tolerance models.

Clone 1G9 is most commonly used as an anti-mouse TIGIT monoclonal antibody, targeting the immunoregulatory protein TIGIT on T and NK cells. In the literature, several other antibodies or proteins are frequently used alongside 1G9, largely because TIGIT biology is intimately connected to related checkpoint proteins and their ligands in immunological research, particularly cancer and autoimmunity studies.

The most commonly used antibodies/proteins with 1G9 include:

• Anti-PD-1 (Programmed cell death protein 1) and anti-PD-L1 (Programmed death ligand 1):Researchers often explore immune checkpoint blockade by combining TIGIT and PD-1/PD-L1 antagonists to examine synergy in tumor suppression or immune modulation.

• Anti-CD226 (DNAM-1):Because DNAM-1 (CD226) is a co-activating receptor that shares ligands (CD112 and CD155) with TIGIT and exhibits counter-regulatory function, studies often measure or block DNAM-1 signaling in parallel with TIGIT to dissect their distinct effects on immune cell activation.

• Ligands: CD155 (PVR) and CD112 (PVRL2):These are the principal ligands for TIGIT and DNAM-1; detection or functional blocking antibodies/proteins against these ligands are frequently used to assess the consequences of interfering with the TIGIT-CD155 axis.

• Anti-CD96 (TACTILE):Like TIGIT, CD96 interacts with CD155 and is another checkpoint under investigation; studies may use anti-CD96 in multiplex approaches with 1G9 when mapping regulatory pathways.

Summary Table: Common Antibodies/Proteins Used with 1G9

Additional context:

• Flow cytometry panels and functional assays using 1G9 will typically include markers for T cells (CD3, CD4, CD8), NK cells (NK1.1, CD49b), and regulatory T cells (FoxP3, CD25) to define affected populations.
• In cancer and autoimmunity research, anti-TIGIT (1G9) is almost always used in the context of multicolor immunophenotyping or functional checkpoint blockade assays that require comprehensive immune monitoring.

According to reagent suppliers and published reviews on TIGIT biology, these combinations are standard in the literature using the 1G9 clone antibody.

Key Findings of Clone 1G9 Anti-TIGIT Antibody in Scientific Literature

Agonistic Activity and T Cell Modulation

• Clone 1G9 is an agonistic anti-mouse TIGIT antibody that fully blocks the binding of TIGIT to its high-affinity ligand CD155 (PVR), demonstrating high specificity for mouse TIGIT.
• In vivo, clone 1G9 exhibits agonistic activity, leading to reduced T cell expansion and decreased production of pro-inflammatory cytokines (e.g., IFN-γ and IL-17), particularly in models of antigen-specific T cell recall responses.
• While clone 1G9 does not directly affect T cell proliferation in vitro, it significantly reduces antigen-specific proliferation and cytokine secretion upon antigen re-stimulation in treated mice, though to a lesser extent than clone 4D4.
• EAE Models: Treatment with clone 1G9 reduces disease severity in experimental autoimmune encephalomyelitis (EAE) models, correlating with decreased Th17 cell frequencies in the central nervous system (CNS).
• No Cell Depletion: Clone 1G9 does not deplete TIGIT-expressing cells in vivo under steady-state conditions, distinguishing it from antibody-dependent cell depletion strategies.

Functional Specificity and Mechanism

• High Specificity: Clone 1G9 was generated by immunizing TIGIT knockout mice with recombinant mouse TIGIT tetramers, followed by extensive screening for TIGIT-specific binding using ELISA and flow cytometry.
• Mechanism: The agonistic activity of clone 1G9 in vivo likely results from stabilizing inhibitory TIGIT signaling, thus dampening T cell activation and inflammatory responses, rather than blocking TIGIT function (as seen with clone 1B4, which acts as a blocking antibody and exacerbates disease).
• TIGIT as Immune Checkpoint: TIGIT is an immune checkpoint receptor expressed on NK cells, activated and memory T cells, and a subset of regulatory T cells. Targeting TIGIT, especially in combination with PD-1/PD-L1 blockade, is considered a promising strategy for immunotherapy.

Contrast with Other Clones

Summary Table of Key Effects

• Reduces T cell expansion and pro-inflammatory cytokine production in vivo.
• Attenuates autoimmune disease severity (EAE) by reducing Th17 cell infiltration.
• Does not affect T cell proliferation in vitro, nor deplete TIGIT+ cells in vivo.
• Fully blocks TIGIT:CD155 interaction without cell depletion.

Conclusion

Clone 1G9 is a well-characterized, agonistic anti-mouse TIGIT monoclonal antibody that modulates immune responses by suppressing T cell activation and cytokine production in vivo, without depleting TIGIT-expressing cells. Its therapeutic potential is highlighted by reduced severity in autoimmune models, making it a valuable tool for studying TIGIT biology and for exploring immunotherapeutic strategies targeting this checkpoint.

Dosing regimens of the anti-mouse TIGIT antibody clone 1G9 vary depending on the mouse model and experimental context, with doses typically ranging from 200 μg to 400 μg per mouse, and the schedule tailored to disease kinetics and study aims.

• In a sepsis model (cecal ligation and puncture, CLP), 1G9 was administered subcutaneously at 400 μg per mouse 1 hour after CLP, with a second injection 12 hours later.
• In an experimental autoimmune encephalomyelitis (EAE) model (a T cell-driven autoimmunity model), 200 μg per mouse intraperitoneally was used, administered on days 0, 2, and 4 after immunization.
• Commercial and scientific overviews confirm no fixed standardized dosing guide exists for clone 1G9 across all models; choices are adjusted according to disease kinetics and experimental aims.

Key points:

• Dose: Common regimens range from 200 μg to 400 μg per mouse per dose.
• Administration route: Both subcutaneous (s.c.) and intraperitoneal (i.p.) injections are used, depending on the study.
• Schedule: Dosing can be once, 12 hours apart, or multiple times (e.g., every other day) based on disease model and experimental design.
• Model-specific adjustments: Dosing and scheduling are adapted for acute (e.g., sepsis) and chronic (e.g., autoimmunity, tumor) models, reflecting differences in antibody clearance and disease progression rates.

No data in the provided sources indicate lower threshold doses (e.g., 5 μg) for 1G9; the lowest and most common effective doses reported are in the 200–400 μg range.

If your application or disease model differs—for example, in oncology or infection—dosing regimens might need further adjustment, usually within the published range and based on factors such as disease kinetics, antibody half-life, and the readout of interest.