The landscape of TIGIT target and clinical application in diseases

Abstract

Immune checkpoint blockade has dramatically altered the concept of cancer therapeutics over the past few years. Beyond the existing classical pathways, novel immune checkpoints, such as T‐cell immunoglobulin and immunoreceptor tyrosine‐based inhibitory motif (ITIM) structural domain (TIGIT), have also emerged in recent years and have promising therapeutic potential. Recent researches have provided ample evidence that TIGIT is extensively involved in various cancerous and noncancerous diseases such as chronic inflammation, autoimmune diseases, abnormal pregnancy status, and most recently coronavirus disease 2019. In contrast to the programmed cell death receptor 1 pathway which primarily affects T‐cell function, targeting TIGIT pathway regulates multiple types of immunocytes but has fewer immune‐related adverse events. Owing to its unique advantages and extensive involvement in diseases, extensive clinical trials blockade TIGIT or combine it with other targets are ongoing, and numerous phase II clinical trials have already seen promising results. In this review, we summarized the existing research on TIGIT in various diseases and discussed the perspective and challenges related to targeting this molecular for therapy, with an attempt to provide directions for subsequent studies.

Advances in Hodgkin Lymphoma Treatment: From Molecular Biology to Clinical Practice

“…TIGIT can be targeted by selective compounds such as the anti-TIGIT humanized mAb vibostolimab, resulting in effective antitumor responses against both solid tumors and hematological neoplasms [100]. Anti-TIGIT and anti-PD-1 drugs have shown in vitro and in vivo synergic action [101]. A phase II study aimed to evaluate the safety and efficacy of the combination pembrolizumabvibostolimab in patients with cHL, NHLs and multiple myeloma is ongoing [102].…”

Single cell immunoprofile of synovial fluid in rheumatoid arthritis with TNF-α/JAK inhibitor treatment

“…5e). Interestingly, the classic exhaustion-related genes were highly enriched in CXCL13 + CD4 + T cells, such as HAVCR2, TIGIT, LAG3, and PDCD1 [46,47] (Fig. 5b).…”