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Times Cited: 17
Times Cited
Times Co-cited
Similarity
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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Developmental Relationships of Four Exhausted CD8+ T Cell Subsets Reveals Underlying Transcriptional and Epigenetic Landscape Control Mechanisms.
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The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells.
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CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer.
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Defining CD8+ T cells that provide the proliferative burst after PD-1 therapy.
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Subsets of exhausted CD8+ T cells differentially mediate tumor control and respond to checkpoint blockade.
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TOX reinforces the phenotype and longevity of exhausted T cells in chronic viral 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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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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T-bet and Eomes are differentially linked to the exhausted phenotype of CD8+ T cells in HIV 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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Early precursor T cells establish and propagate T cell exhaustion in chronic infection.
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CD4+ T Cell Help Is Required for the Formation of a Cytolytic CD8+ T Cell Subset that Protects against Chronic Infection and Cancer.
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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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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.