IL15 and TIGIT blockade enhances the natural killer (NK) cell-mediated activity against MHC-I-deficient melanoma both and in preclinical models. IL15-induced harnessing of NK cells, associated with their unleashing by TIGIT blockade, may represent a therapeutic approach for tumors, which lack HLA-I molecules thus escaping the CD8 T cell-mediated control..
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Background: PD-L1 and VEGF blockade with atezolizumab plus bevacizumab has been shown to improve survival in unresectable hepatocellular carcinoma. TIGIT is an immune checkpoint regulator implicated in many cancers, including unresectable hepatocellular carcinoma. Here, we evaluate the clinical activity and safety of the addition of tiragolumab, an anti-TIGIT monoclonal antibody, to atezolizumab plus bevacizumab.
View Article and Find Full Text PDFTIGIT and PVRIG are immune checkpoints co-expressed on activated T and NK cells, contributing to tumor immune evasion. Simultaneous blockade of these pathways may enhance therapeutic efficacy, positioning them as promising dual targets for cancer immunotherapy. This study aimed to develop a bispecific antibody (BsAb) to co-target TIGIT and PVRIG.
View Article and Find Full Text PDFExploring novel immunotherapy in advanced esophageal squamous cell carcinoma: Is targeting TIGIT an answer?
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January 2025
Department of Medical Oncology, National Taiwan University Cancer Center, 7 Chung-Shan South Road, Taipei, 10002, Taiwan.
Esophageal squamous cell carcinoma (ESCC) is a prevalent and highly lethal malignancy in Asia. Recent advancements in immune checkpoint inhibitors (ICIs) have markedly transformed the systemic therapy landscape for ESCC. Anti-PD-1-based combination with chemotherapy or with ipilimumab, an anti-CTLA-4 antibody, have been established as the new standard first-line treatments for patients with advanced ESCC.
View Article and Find Full Text PDFAnti-correlation of KLRG1 and PD-1 expression in human tumor CD8 T cells.
Oncotarget
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Recently, combination checkpoint therapy of cancer has been recognized as producing additive as opposed to synergistic benefit due in part to positively correlated effects. The potential for uncorrelated or negatively correlated therapies to produce true synergistic benefits has been noted. Whereas the inhibitory receptors PD-1, CTLA-4, TIM-3, LAG-3, and TIGIT have been collectively characterized as exhaustion receptors, another inhibitory receptor KLRG1 was historically characterized as a senescent receptor and received relatively little attention as a potential checkpoint inhibitor target.
View Article and Find Full Text PDFPublisher Correction: TIGIT and PD-L1 co-blockade promotes clonal expansion of multipotent, non-exhausted antitumor T cells by facilitating co-stimulation.
Nat Cancer
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Genentech, South San Francisco, CA, USA.
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