TIGIT

Overview

TIGIT (T Cell Immunoreceptor With Ig And ITIM Domains) is an inhibitory immune checkpoint receptor expressed on T cells and NK cells. It competes with the co-stimulatory receptor CD226 (DNAM-1) for binding to CD155 (PVR) and CD112 (PVRL2) on tumor and antigen-presenting cells. TIGIT has emerged as a major co-inhibitory axis in tumor immunity, and its selective upregulation on tumor-infiltrating lymphocytes in responders to checkpoint blockade makes it a candidate for combination immunotherapy strategies.

Alterations observed in the corpus

• Selectively upregulated on-therapy in nivolumab responders (vs non-responders) in melanoma; nominated by transcriptomic analysis as a candidate target for combination immunotherapy PMID:29033130.

Cancer types (linked)

• MEL (Melanoma) — TIGIT expression increased on-therapy in nivolumab-treated melanoma patients who responded; nominated alongside TNFRSF4 (OX40), HAVCR2 (TIM-3), and VSIR (VISTA) as a combination target PMID:29033130.

Co-occurrence and mutual exclusivity

• Co-upregulated on-therapy with other checkpoint receptors TNFRSF4 (OX40), HAVCR2 (TIM-3), VSIR (VISTA), LAG3, TNFRSF9 (4-1BB), and ICOS in responders PMID:29033130.

Therapeutic relevance

• Anti-TIGIT antibodies are in clinical development for combination with PD-1/PD-L1 blockade; on-therapy induction in nivolumab responders provides biological rationale for anti-PD-1 + anti-TIGIT combination in melanoma PMID:29033130.

Open questions

• Whether pre-therapy TIGIT expression level or baseline tumor infiltration is predictive of anti-PD-1 response remains uncharacterized in this cohort PMID:29033130.

Sources

• PMID:29033130

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