TIGIT Antibodies

T-cell immunoreceptor with Ig and ITIM domains (TIGIT)

Binds with high affinity to the poliovirus receptor (PVR) which causes increased secretion of IL10 and decreased secretion of IL12B and inhibits T-cell activation by promoting the creation of mature immunoregulatory dendritic cells. .

Gene Information

Human
Gene Name:	TIGIT
Uniprot:	Q495A1
Entrez:	201633

Family

Belongs to:
No superfamily

Alternative Names

T cell immunoreceptor with Ig and ITIM domains; TIGIT; VSIG9; VSTM3; WUCAM

Molecular Weight

Mass (kDA):
26.319 kDA

Genomic Context

Human
Location:	3q13.31
Sequence:	3; NC_000003.12 (114291102..114329747)

Tissue Specificity

Expressed at low levels on peripheral memory and regulatory CD4+ T-cells and NK cells and is up-regulated following activation of these cells (at protein level).

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein.

Diseases

• Autoimmune Diseases
• Autoimmune Reaction
• Neoplasms
• Autoimmunity
• Tissue Adhesions
• Sclerosis
• Chronic Infectious Disease
• Hepatitis
• Hepatitis C, Chronic
• Multiple Sclerosis
• Autoimmune Diseases Of The Nervous System
• Hepatitis C

• Experimental Autoimmune Encephalomyelitis
• Virus Diseases
• Delayed Hypersensitivity
• Malignant Neoplasms
• Nervousness
• Viremia

Interacting Proteins

• CD226
• NECTIN2
• NECTIN3
• NECTIN4
• PVR

Pathways

• Cell Activation
• Cell Proliferation
• T Cell Activation
• Immune Response
• Cytokine Production
• T Cell Proliferation
• Cell Differentiation
• Cell Adhesion
• Cell-cell Signaling
• Tissue Morphogenesis

• Receptor Clustering
• Hypersensitivity
• Humoral Immune Response
• Cell-cell Adhesion

PTMs

• Phosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TIGIT

Best Uses of the TIGIT Marker

We will be discussing the numerous uses of the TIGIT marker. This includes its inhibitory role , as T cell activation is slowed and its ability to inhibit auto-pathogenic TH2/TH27 T cells responses. In addition, we will discuss the role that TIGIT plays in cytotoxicity as well as anti-tumor responses. Below are the best uses of this marker. Continue reading to find out more.

TIGIT is a key mediator of T-cell activation

TIGIT is a co-inhibitor for T-cell activation. It binds with CD226 and blocks its stimulatory functions. T cells are essential for the immune system's ability monitor and respond to pathogens and invaders. TIGIT has multiple biological effects, such as the reduction of T cell proliferation as well as toxicity, as well as reducing dendritic cell cytokine production.

TIGIT is a molecule that inhibits checkpoints that has recently been implicated in the field of tumor immunosurveillance. It is only weakly expressed on naive cells, however, it is highly induced when exposed to antigen-specific stimuli. It binds to CD155 CD112 (PVRL2) and nectin-2. It competes against CD226 (PVR), CD112 (PVRL2) and nectin-2 to bind to immune cells' surfaces.

Scientists utilized a polypeptide sequence from the human g1 heavy-chain gene (hTIGITFc) to select the phage with high affinity for TIGIT. Each phage has a distinct light-chain variable region. This is the basis for the creation of a new library of phages.

Antibodies against TIGIT are created by merging the constant and variable regions of the antibodies. The desired cytotoxicity determines which regions are selected. IgG1 & IgG3 have cytotoxicity that is mediated by complement. IgG2 & IgG4 do not. Light chain constant regions can be lambda, kappa or a combination of both. Attenuated human IgG1 will be the most appropriate for immunotherapy purposes.

TIGIT antibodies are a good choice to use in conjunction with other drugs or treatments for the immune system. This treatment can reduce the dosage of another drug or reduce the effects. Combination therapy may create synergistic effects on T-cell activation. T-cell activation can be achieved with two different antibodies. One is a monoclonal one, and the other is a polyclonal antibody.

It inhibits auto-pathogenic TH2/TH27 T cell responses

The TIGIT gene has the ability to recognize a subset of human T cells that function distinct from TH2 cells. Although these cells are believed to play a role in autoimmunity, and their function is not fully understood, they are thought to play an important role. They can switch from TH2 cells to non-TH2 cells. Additionally, this type of T cells is associated with many chronic illnesses, such as autoimmune arthritis, also known as rheumatoid.

The team's research revealed 7401 proteins that were found in blood, tissues and lymphocytes of patients with TH2/TH27 cancer. 334 of these proteins were differentially expressed between the two types of cells. Significant differences were found in the expression of cytotoxic protein in TH2 clones. Additionally, a flow cytometry analysis revealed that TH2 cells express more chemical cytotoxic substances.

The study also compared the effects of proinflammatory cytokines synoviocytes versus endothelial cells. T-cell clones of both the TH2/TH27 and TH27 lineages were shown to increase their productions of IL-6. These cells, therefore, inhibit the auto-pathogenic TH2/TH27 T cells.

TIGIT is a binder for the transforming growth factor beta or TGF-beta. It reduces the proliferation of antigen-specific CD4+ human T cells. TGF-beta inhibits the secretion of IL-12, the cytokine that drives auto-pathogenic TH2/TH27 T cells. The TIGIT molecules also block the production of the cytokine IFN-g that is associated with inflammation.

TIGIT peptides are required for a precise measurement of auto-pathogenic TH2/TH27 T cells. The peptide TIGIT not only inhibits auto-pathogenic TH2 T cell responses, but also decreases TH27 expression and increases FOXP3 expression. In a mouse model, this peptide has been shown to block autopathogenic TH2/TH27 responses.

It can result in cytotoxicity

TIGIT is a inhibitory molecular that regulates the immune response by sending inhibitory signals to effector T and NK cells. It also boosts Tregs' suppressive power. TIGIT isn't found in all tissues. Despite its importance, the molecular mechanisms underlying its actions aren't fully understood. TIGIT has been identified as a potential therapeutic target.

The study employed CD155-expressing tumor cells in co-culture with CD19 CAR T-cells. In co-culture studies, TIGIT-28 increased the production of cytokines. In co-cultures with K562-CD19/155-expressing target cells, TIGIT-28 promoted 50% higher TNFa secretion than the control group. TIGIT-28 was not able to increase TNFa secretion in cocultures with CD155-negative targets.

The anti-TIGIT Abs derived in the present study show limitations in their functional properties in vitro. However, the study showed the existence of two monoclonal anti-TIGIT Abs. These antibodies can be used in in vivo studies to manipulate TIGIT function. It is important to remember that the study didn't reveal any distinction in the lesions of antagonistic and agonistic anti-TIGIT Abs treatment in TIGIT mice. However the results were in agreement with the agonistic antibodies and anti-TIGIT Abs decreased the frequency of IL-17+ TH27 cells in CNS. Therefore, it is crucial to know that the functional modulation of T-cell responses is reflected in a difference in the severity of disease during EAE.

A study using mice transgenic for BosterBio's TIGIT marker was conducted. It showed that the antigen can boost both CD4- and CD8 T cell function. TIGIT-28 also increases the cytotoxicity in antigen-infected F4 T cells. The study also revealed that TIGIT-28 may be able to enhance the function of CD8+ T cells.

It blocks anti-tumor immune responses.

TIGIT is a protein that blocks immune responses to cancer by reducing T cell activation and inducing regulatory cells. It hinders the immune system's cycle of proinflammatory T cell responses. TIGIT is present on both CD4+ and CD8+ T cell lines, and it inhibits both types of immune responses in cancer. The exact role it plays in immunotherapy for cancer remains unclear.

Researchers have found that the TIGIT28 protein improves CD8 and CD4 T-cell function by inhibiting the expression of the PD-L1 gene. TIGIT28-expressing T-cells also have better functions than T-cells that did not express the T-cell antigen CD69. These immune cells can also be stimulated by a new anti-tumor treatment.

TIGIT is a crucial cancer antigen. T-cells that express it produce a protein that resembles chemokine. Anti-TIGIT antibodies trigger the cells to produce chemicals. TIGIT is expressed on both CD8 T cells and Tregs. TIGIT could be responsible to block antitumor responses in different types of cancers.

In addition to interfacing with T-cells, anti-TIGIT antibodies could also interact with other checkpoint inhibitors to enhance immune responses against tumors. A number of these agents are currently being studied in combination, but more studies are needed to prove their effectiveness. The potential is huge for this drug. Clinical trials are the only way to test its effectiveness.

T-cells can be evaded by anti-TIGIT antibodies. These agents effectively block T-cell activation through targeting the T-cell antigen. Using this antibody can prevent the immune response to tumors in mice. This approach could be used to develop effective anti-tumor therapies. Anti-TIGIT T cells can block the immune system mediated by PD-1 in mice.

It helps prevent graft-versus-host disease.

CD155, is a CD8(+) T cell, is a marker for TIGIT. In graft versus host disease, T cells detect CD155 and respond by blocking the immune system from activating the graft. This is a positive change, as it could potentially help in understanding the causes of GVHD and its therapeutic potential.

TIGIT is a protein that can be found in a variety of tumors but is most relevant to triple-negative breast cancer. This tumor type is a great candidate for immunotherapy as TIGIT is very prevalent in malignant breast tissue. This is important because malignant breast tissue expresses higher levels of TIGIT than normal breast tissue, highlighting the potential for targeted therapies targeting TGIT.

TIGIT Fc decreased small intestinal and liver tissue injury and lymphocytic invasion. Additionally, TIGIT-Fc slowed CD8+ T cell activation in vitro. TIGIT-CD155 was associated with Erk phosphorylation and STAT3 nuclear translocation, and STAT3 nuclear mechanisms that contribute towards GVHD.