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

Clone 1G9 is commonly applied in vivo in mice for the blockade or agonistic modulation of TIGIT, a key immune checkpoint molecule that regulates T and NK cell activity. The primary use is to investigate TIGIT’s role in immune regulation, inflammation, and autoimmunity.

Essential context and supporting details:

• Immune checkpoint studies: 1G9 is used to block the interaction between TIGIT and its ligand CD155, thereby modifying T cell proliferation, cytokine production, and immune responses in mouse models. This allows researchers to study TIGIT’s function in immune tolerance, tumor immunity, and autoimmunity.
• Autoimmune disease models: Administration of 1G9 suppresses T cell-driven inflammation, making it a valuable tool in experimental models of autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE) and colitis. It is noted for promoting immune regulation rather than depleting TIGIT+ cells.
• Functional blockade: 1G9 acts as a blocking antibody for mouse TIGIT and is used for in vivo TIGIT inhibition to examine biological effects on various T cell subsets, including regulatory T cells (Tregs), CD4+, and CD8+ populations.
• Flow cytometry and tissue analysis: Beyond functional studies, 1G9 is frequently used for the detection and characterization of TIGIT-expressing cells in tissues.

Other relevant information:

• 1G9 does not deplete TIGIT+ cells under steady-state conditions but instead modulates their function.
• It is generated from TIGIT−/− mice immunized with TIGIT and is a mouse IgG1 isotype, making it suitable for sustained in vivo use without producing anti-hamster antibody responses.

In summary, clone 1G9 is a widely used tool for in vivo studies of TIGIT function in murine models, particularly for immune regulation, autoimmune disease research, and checkpoint blockade experimentation.

Some of the most commonly used antibodies or proteins with 1G9 (which is specific for mouse TIGIT) in immunological literature are other immune checkpoint molecules and their ligands, particularly those involved in T cell regulation and cancer immunotherapy research. The most frequently co-used targets include:

• PD-1 (Programmed cell death protein 1) and PD-L1 (Programmed death-ligand 1):
  • TIGIT and the PD-1/PD-L1 pathway are often targeted simultaneously to investigate their additive or synergistic roles in tumor suppression and immunotherapy. Experiments typically include anti-PD-1 and/or anti-PD-L1 antibodies when using 1G9.
• CD155 (PVR) and CD112 (PVRL2):
  • These are the core ligands for TIGIT and are routinely assessed in mechanistic studies using 1G9 to block or detect TIGIT-ligand interactions.
• CD226 (DNAM-1) and CD96 (TACTILE):
  • These receptors are part of the same pathway and compete with TIGIT for binding to CD155 and CD112. Their expression is often analyzed or blocked alongside 1G9 to dissect the balance of activating versus inhibitory signaling on T cells and NK cells.
• Other immune cell markers: For functional analysis, antibodies against CD3, CD4, CD8, NK1.1, and regulatory T cell markers (such as Foxp3) are commonly used with 1G9 to identify and characterize specific immune cell populations responding to TIGIT signaling.
• Isotype control antibodies: Mouse IgG1 κ isotype controls matching 1G9 are typically included to validate specificity in flow cytometry and in vivo experiments.

Typical applications where these are combined include flow cytometry, immunofluorescence, ELISA, and in vivo checkpoint blockade or mechanistic studies in mouse models.

In summary, studies using 1G9 (anti-mouse TIGIT) most often combine it with anti-PD-1/PD-L1, ligands CD155 and CD112, other checkpoint/immune receptors (CD226, CD96), and standard immune cell surface markers. This combination allows for comprehensive profiling of immune checkpoint interactions and functional assessments in cancer, infection, and autoimmunity research.

Key findings from scientific literature regarding clone 1G9 focus on its specificity, mechanism of action, functional impact, and experimental use in mouse models:

• Specificity and Blocking Capacity: Clone 1G9 is a monoclonal antibody directed specifically against mouse TIGIT (T cell immunoreceptor with Ig and ITIM domains). It fully blocks the interaction between TIGIT and its high-affinity ligand CD155 (also known as PVR).

• Functional Modulation: 1G9 displays agonistic anti-TIGIT activity in vivo. It can suppress T cell expansion and pro-inflammatory cytokine production during immune responses. In vivo studies demonstrate that 1G9 treatment reduces the severity of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, mainly by reducing the frequencies of IL-17^+^ Th17 cells in the central nervous system.

• Effect on T Cell Proliferation: In vitro, clone 1G9 does not significantly affect T cell proliferation. Its prominent immune-modulating effects are observed under in vivo conditions, especially during immune challenges such as autoimmunity or infection.

• Experimental Evidence:

  • In EAE models, 1G9 reduced antigen-specific T cell proliferation and effector cytokine (IFN-γ and IL-17) secretion compared to controls.
  • 1G9 was as effective or more effective than related agonistic clones in reducing disease severity in chronic experimental settings.
  • Unlike some anti-TIGIT antibodies that deplete TIGIT^+^ cells, 1G9 does not deplete these cells under steady-state conditions.

• Research Utility: Clone 1G9 is widely used for functional assays (such as ELISA, flow cytometry, and immunofluorescence) to study TIGIT's role in immunoregulation, checkpoint pathways, and experimental immunotherapy models.

• TIGIT Biology Context: TIGIT is an immune checkpoint receptor present on NK cells, activated T cells, memory T cells, and a subset of regulatory T cells. It inhibits immune cell responses and is targeted in cancer immunotherapy and autoimmune disease research.

• Citation Highlights:

  • Clone 1G9 is repeatedly cited in the context of mouse immunology as an agonistic antibody that functionally mimics TIGIT signaling, modulates immune responses, and serves as a preclinical tool for dissecting checkpoint pathways.

In sum, clone 1G9 is a validated, in vivo agonist anti-TIGIT antibody that is broadly used to block TIGIT-CD155 binding, to probe TIGIT's suppressive signaling, and to dissect the role of TIGIT in mouse models of autoimmunity and cancer.

Dosing regimens of clone 1G9 (anti-mouse TIGIT antibody) show significant variation depending on the mouse disease model, experimental timing, and measured endpoints, with no universal standardized regimen across studies. The principal factors influencing these regimens are disease kinetics and experimental objectives.

Reported 1G9 dosing regimens across mouse models:

• Sepsis Model (CLP):

  • Dose: 400 μg per mouse, administered subcutaneously 1 hour after cecal ligation and puncture (CLP), and repeated 12 hours later.
  • Purpose: To modulate immune dysregulation and improve survival in sepsis.

• Experimental Autoimmune Encephalomyelitis (EAE) Model:

  • Dose: 200 μg per mouse, administered intraperitoneally on days 0, 2, and 4 after disease induction.
  • Purpose: To reduce disease severity by acting as an agonist on TIGIT and modulating T cell responses.

• General Guidance and Manufacturer Recommendations:

  • Route: Both intraperitoneal (i.p.) and subcutaneous (s.c.) routes have been used, with intraperitoneal being common.
  • Frequency: Depending on the model, may range from single or dual acute dosing (sepsis) to repeated dosing every other day or at induction and during early disease (EAE).
  • According to manufacturers, regimens should be tailored to the experimental aim as no standardized guide exists for all models.

Summary Table: Common Dosing Regimens of Clone 1G9 in Mouse Models

Additional Considerations:

• The optimal regimen depends on the disease context, antibody purpose (agonist vs. blocking), and experimental endpoints (acute vs. chronic).
• Always refer to published studies specific to the disease model and antibody supplier technical data for optimization.
• Published protocols indicate dosing between 200–400 μg per mouse per injection is typical, using i.p. or s.c. routes, with timing and frequency customized per study.

In summary, the dosing regimen of clone 1G9 is not fixed but is instead adapted to the mouse model, disease kinetics, and study aims, with acute disease models such as sepsis using higher, closely-timed doses, and chronic models such as EAE using moderate, spaced-out regimens.