TOX-expressing terminally exhausted tumor-infiltrating CD8+ T cells are reinvigorated by co-blockade of PD-1 and TIGIT in bladder cancer

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TOX is expressed by exhausted and polyfunctional human effector memory CD8+ T cells

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Human effector T cells express TOX—Not so “TOX”ic after all

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TOX promotes the exhaustion of antitumor CD8+ T cells by preventing PD1 degradation in hepatocellular carcinoma

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TOX reinforces the phenotype and longevity of exhausted T cells in chronic viral infection

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TOX is a critical regulator of tumour-specific T cell differentiation

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TOX transcriptionally and epigenetically programs CD8+ T cell exhaustion

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Single-cell RNA-seq reveals TOX as a key regulator of CD8+ T cell persistence in chronic infection

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TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion

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VEGF-A drives TOX-dependent T cell exhaustion in anti–PD-1–resistant microsatellite stable colorectal cancers

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Co-expression of CD39 and CD103 identifies tumor-reactive CD8 T cells in human solid tumors

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Association Between Expression Level of PD1 by Tumor-Infiltrating CD8+ T Cells and Features of Hepatocellular Carcinoma

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T-Cell Immunoglobulin and ITIM Domain (TIGIT) Associates with CD8+ T-Cell Exhaustion and Poor Clinical Outcome in AML Patients

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TIGIT and PD-1 impair tumor antigen–specific CD8+ T cells in melanoma patients

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The Immunoreceptor TIGIT Regulates Antitumor and Antiviral CD8 + T Cell Effector Function

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Progenitor and Terminal Subsets of CD8+ T Cells Cooperate to Contain Chronic Viral Infection

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Transcription factor T-bet represses expression of the inhibitory receptor PD-1 and sustains virus-specific CD8+ T cell responses during chronic infection

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The surface protein TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells

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