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The epigenetic landscape of T cell exhaustion.
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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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Subsets of exhausted CD8+ T cells differentially mediate tumor control and respond to checkpoint blockade.
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TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion.
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The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells.
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Chromatin states define tumour-specific T cell dysfunction and reprogramming.
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The TCF1-Bcl6 axis counteracts type I interferon to repress exhaustion and maintain T cell stemness.
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PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression.
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Tumor-Specific T Cell Dysfunction Is a Dynamic Antigen-Driven Differentiation Program Initiated Early during Tumorigenesis.
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Bioenergetic Insufficiencies Due to Metabolic Alterations Regulated by the Inhibitory Receptor PD-1 Are an Early Driver of CD8(+) T Cell Exhaustion.
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T-cell exhaustion, co-stimulation and clinical outcome in autoimmunity and infection.
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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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Progressive loss of memory T cell potential and commitment to exhaustion during chronic viral infection.
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Transcription Factor IRF4 Promotes CD8+ T Cell Exhaustion and Limits the Development of Memory-like T Cells during Chronic Infection.
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T cells maintain an exhausted phenotype after antigen withdrawal and population reexpansion.
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Defining 'T cell exhaustion'.
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Proliferating Transitory T Cells with an Effector-like Transcriptional Signature Emerge from PD-1+ Stem-like CD8+ T Cells during Chronic Infection.
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De Novo Epigenetic Programs Inhibit PD-1 Blockade-Mediated T Cell Rejuvenation.
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T-cell invigoration to tumour burden ratio associated with anti-PD-1 response.
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Selective expansion of a subset of exhausted CD8 T cells by alphaPD-L1 blockade.
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T cell costimulatory receptor CD28 is a primary target for PD-1-mediated inhibition.
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Follicular CXCR5- expressing CD8(+) T cells curtail chronic viral infection.
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CD8 T Cell Exhaustion in Chronic Infection and Cancer: Opportunities for Interventions.
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Developmental Relationships of Four Exhausted CD8+ T Cell Subsets Reveals Underlying Transcriptional and Epigenetic Landscape Control Mechanisms.
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Rescue of exhausted CD8 T cells by PD-1-targeted therapies is CD28-dependent.
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Tumor antigen-specific CD8 T cells infiltrating the tumor express high levels of PD-1 and are functionally impaired.
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Viral antigen and extensive division maintain virus-specific CD8 T cells during chronic infection.
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TCF-1-Centered Transcriptional Network Drives an Effector versus Exhausted CD8 T Cell-Fate Decision.
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The immunoreceptor TIGIT regulates antitumor and antiviral CD8(+) T cell effector function.
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Bystander CD8+ T cells are abundant and phenotypically distinct in human tumour infiltrates.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.