Human TIGIT Protein
- Known as:
- Human TIGIT Protein
- Catalog number:
- TIT-H52H3
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human TIGIT Protein
Related genes to: Human TIGIT Protein
- Gene:
- TIGIT NIH gene
- Name:
- T cell immunoreceptor with Ig and ITIM domains
- Previous symbol:
- VSIG9, VSTM3
- Synonyms:
- FLJ39873, DKFZp667A205
- Chromosome:
- 3q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-07
- Date modifiied:
- 2017-12-06
Related products to: Human TIGIT Protein
Related articles to: Human TIGIT Protein
- Glioma is an aggressive brain malignancy characterized by a markedly immunosuppressive microenvironment and limited response to conventional treatments. CD155, also known as the poliovirus receptor, is frequently overexpressed in glioma and plays a key role in immune escape. By interacting with inhibitory receptors such as TIGIT and CD96, as well as the activating receptor CD226, CD155 modulates the tumor immune landscape. These interactions suppress the cytotoxic activity of T cells and natural killer (NK) cells while promoting immunoregulatory phenotypes, thereby impairing immune-mediated tumor cell elimination and supporting tumor progression. The balance among these receptor-ligand interactions is critical in determining immune outcomes. Targeting the CD155 axis has emerged as a potential therapeutic strategy. Approaches including monoclonal antibodies, bispecific antibodies, and chimeric antigen receptor (CAR)-engineered immune cells are being developed to counteract immune suppression and restore antitumor responses. This review summarizes the structural and functional features of CD155 and its associated receptors, examines their roles in glioma immune evasion, and discusses recent advances and challenges in developing therapies targeting this pathway. Modulation of CD155-related signaling may offer new opportunities to improve treatment outcomes in glioma. - Source: PubMed
Publication date: 2026/05/22
Huang MingyaoCui YouchenWang XiaoqianWeng YangHuang HuiyanSu WeiweiZhao ShanLi Yan - Regulatory T cells (Tregs) play a critical role in maintaining immune homeostasis and tolerance. While their suppressive function is beneficial in autoimmunity and detrimental in cancer, Tregs also exert essential roles during infections where their functions are nuanced and depend on the context, making their overall role more complex to understand. During infections, Tregs classically dampen excessive immune activation, but this suppression may also allow pathogen persistence. In addition to suppressing excessive inflammation, Tregs can directly promote tissue repair and protection. Recent findings demonstrate that these regenerative properties are also important during infections, where limiting immunopathology and promoting repair are both critical to recovery. Moreover, immune checkpoint molecules such as TIM-3 and TIGIT, classically associated with Treg-mediated suppression, have recently also been suggested to contribute to tissue protection or active repair. Their expression on Tregs raises the possibility that these molecules may support functions beyond immune regulation, potentially participating in the orchestration of tissue repair. This review will focus on how Tregs balance immune suppression and tissue repair during infections, highlighting the importance of these functions for recovery and their potential in developing new therapeutic strategies. - Source: PubMed
Publication date: 2025/11/29
Hilaire MorganeJoller Nicole - Acquired resistance (AR) to immune checkpoint inhibitors (ICIs) remains a major obstacle to durable clinical benefit in non-small cell lung cancer (NSCLC). Emerging after initial responses, AR reflects tumor evolution, immune escape, and metabolic reprogramming. Key mechanisms may include impaired antigen presentation (β2-microglobulin, human leukocyte antigen mutations), T-cell exhaustion, and remodeling of the tumor microenvironment (TME). In this review, we summarize the current understanding of ICIs resistance and highlight therapeutic strategies under investigation to overcome it. Novel approaches include next-generation ICIs targeting TIGIT and LAG-3, epigenetic modulators (HDAC, DNMT inhibitors), and metabolic agents relevant to and mutations. Additional strategies aim to reprogram the TME through AXL or multikinase inhibition, tumor-treating fields, and cytokine- and/or gene-based therapies. Cellular immunotherapies (tumor-infiltrating lymphocytes, T-cell receptors, chimeric antigen receptor-T), antibody-drug conjugates, and vaccines offer complementary means to restore antitumor immunity. Advancing the field will require biomarker-driven patient selection and rational combinations to overcome AR and achieve more durable, personalized immunotherapy outcomes in NSCLC. - Source: PubMed
Publication date: 2026/05/22
Hidalgo-Filho Cassio MuriloSanto ValentinaGariazzo EleonoraAldea MihaelaPecci FedericaDanlos François-Xavierde Castro Junior GilbertoRicciuti Biagio - Combinations of anti-PD-1/PD-L1 immunotherapy (IO) and anti-VEGF tyrosine kinase inhibitor (TKI) are recommended as first-line therapy for metastatic renal cell carcinoma (RCC). We aimed to evaluate the predictive value of tissue factor pathway inhibitor 2 (TFPI2) for IO + TKI response. - Source: PubMed
Publication date: 2026/05/22
Wang JiajunDu LingzhiWang YingWang HangZhu YanjunXu Xianglai - The immune mechanisms underlying chronic obstructive pulmonary disease (COPD) remain incompletely understood, particularly regarding immune checkpoint dysregulation. This cross-sectional observational study aimed to determine whether activation of the T-cell immunoglobulin and ITIM domain (TIGIT) pathway contributes to CD8-positive T-cell exhaustion and susceptibility to frequent exacerbations in COPD. - Source: PubMed
Publication date: 2026/05/21
Wang DanLi HuiZhao ZhijunZhao JialeHai XiaolanFan YuchunMa WeirongChen JuanGe XiahuiDuan XiangguoHou Jia