TIGIT as an emerging immune checkpoint
Open accessAbstract
Summary: T cell immunoglobulin and ITIM domain (TIGIT) is an inhibitory receptor expressed on lymphocytes that was recently propelled under the spotlight as a major emerging target in cancer immunotherapy. TIGIT interacts with CD155 expressed on antigen-presenting cells or tumour cells to down-regulate T cell and natural killer (NK) cell functions. TIGIT has emerged as a key inhibitor of anti-tumour responses that can hinder multiple steps of the cancer immunity cycle. Pre-clinical studies indicated that TIGIT blockade may protect against various solid and haematological cancers. Several monoclonal antibodies (mAbs) that block the inhibitory activity of human TIGIT have been developed. Clinical trials are ongoing, investigating TIGIT blockade as a monotherapy or in combination with anti-PD1/PD-L1 mAbs for the treatment of patients with advanced solid malignancies. In this review, we cover our current knowledge on TIGIT, from its discovery in 2009 to its current status as a clinical target.
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TIGIT inhibits T cell and NK cell activity by interacting with CD155, which is expressed on antigen-presenting cells or cancer cells.
“TIGIT inhibits T cell and NK cell activity by interacting with CD155, which is expressed on antigen-presenting cells (APC) or cancer cells.”
From Mesenchymal stromal cells in bone marrow niche of patients with multiple myeloma: a double-edged sword (2025) · cites this paper as [208]
Cites
The interaction of TIGIT with PVR and PVRL2 inhibits human NK cell cytotoxicity
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Lymphoproliferative Disorders with Early Lethality in Mice Deficient in <i>Ctla-4</i>
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“According to preclinical research, TIGIT blockage may offer protection against several hematological and solid malignancies [208].”
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- Authors
- Harjunpää, H., & Guillerey, C.
- Affiliations
- University of Helsinki (FI)
- Translational Research Institute (AU)
- Corresponding author
- Guillerey, C
- Venue
- Clinical and Experimental Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-12-25
- Volume
- 200
- Issue
- 2
- Pages
- 108-119
- ISSN
- 0009-9104 (ISSN-L)
- 1365-2249
- PMC
- PMC7160651
- OpenAlex
- W2995440672
- Cited by
- 552
- References
- 3
- Citations by year
- 2026: 53 · 2025: 82 · 2024: 98 · 2023: 109 · 2022: 94 · 2021: 79 · 2020: 35 · 2018: 1
- FWCI
- 4.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Clinical & Experimental Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Työväentutkimus Vuosikirja (submittedVersion)
- Funders
- Cancer Australia (1139048)
- National Health and Medical Research Council (1107417)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- TIGIT, immune checkpoint, CD155, T cell inhibitory receptors, NK cell inhibition, cancer immunotherapy, monoclonal antibodies, solid tumors, hematologic malignancies, tumour immunity
- MeSH terms
- Antineoplastic Agents, Immunological, Humans, Killer Cells, Natural, Neoplasm Proteins, Neoplasms, Receptors, Immunologic, Receptors, Virus, T-Lymphocytes
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