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Times Cited: 302
Times Cited: 302
Times Cited
Times Co-cited
Similarity
TOX transcriptionally and epigenetically programs CD8+ T cell exhaustion.
Omar Khan, Josephine R Giles, Sierra McDonald, Sasikanth Manne, Shin Foong Ngiow, Kunal P Patel, Michael T Werner, Alexander C Huang, Katherine A Alexander, Jennifer E Wu,[...]. Nature 2019
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TOX is a critical regulator of tumour-specific T cell differentiation.
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TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion.
Hyungseok Seo, Joyce Chen, Edahí González-Avalos, Daniela Samaniego-Castruita, Arundhoti Das, Yueqiang H Wang, Isaac F López-Moyado, Romain O Georges, Wade Zhang, Atsushi Onodera,[...]. Proc Natl Acad Sci U S A 2019
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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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Defining CD8+ T cells that provide the proliferative burst after PD-1 therapy.
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CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer.
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T Cell Factor 1-Expressing Memory-like CD8(+) T Cells Sustain the Immune Response to Chronic Viral Infections.
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Daniel T Utzschneider, Mélanie Charmoy, Vijaykumar Chennupati, Laurène Pousse, Daniela Pais Ferreira, Sandra Calderon-Copete, Maxime Danilo, Francesca Alfei, Maike Hofmann, Dominik Wieland,[...]. Immunity 2016
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Epigenetic stability of exhausted T cells limits durability of reinvigoration by PD-1 blockade.
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Subsets of exhausted CD8+ T cells differentially mediate tumor control and respond to checkpoint blockade.
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The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells.
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The epigenetic landscape of T cell exhaustion.
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Intratumoral Tcf1+PD-1+CD8+ T Cells with Stem-like Properties Promote Tumor Control in Response to Vaccination and Checkpoint Blockade Immunotherapy.
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Chromatin states define tumour-specific T cell dysfunction and reprogramming.
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Molecular signature of CD8+ T cell exhaustion during chronic viral infection.
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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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TCF-1-Centered Transcriptional Network Drives an Effector versus Exhausted CD8 T Cell-Fate Decision.
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Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection.
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Defining T Cell States Associated with Response to Checkpoint Immunotherapy in Melanoma.
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The TCF1-Bcl6 axis counteracts type I interferon to repress exhaustion and maintain T cell stemness.
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NR4A transcription factors limit CAR T cell function in solid tumours.
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Restoring function in exhausted CD8 T cells 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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Tumor-Specific T Cell Dysfunction Is a Dynamic Antigen-Driven Differentiation Program Initiated Early during Tumorigenesis.
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Follicular CXCR5- expressing CD8(+) T cells curtail chronic viral 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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TOX promotes the exhaustion of antitumor CD8+ T cells by preventing PD1 degradation in hepatocellular carcinoma.
Xiaochen Wang, Qifeng He, Haiyuan Shen, Anliang Xia, Wenfang Tian, Weiwei Yu, Beicheng Sun. J Hepatol 2019
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De Novo Epigenetic Programs Inhibit PD-1 Blockade-Mediated T Cell Rejuvenation.
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Transcriptional control of effector and memory CD8+ T cell differentiation.
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Checkpoint Blockade Immunotherapy Induces Dynamic Changes in PD-1-CD8+ Tumor-Infiltrating T Cells.
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Genome-wide analysis identifies NR4A1 as a key mediator of T cell dysfunction.
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Genetic absence of PD-1 promotes accumulation of terminally differentiated exhausted CD8+ T cells.
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Early precursor T cells establish and propagate T cell exhaustion in chronic infection.
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Dysfunctional CD8 T Cells Form a Proliferative, Dynamically Regulated Compartment within Human Melanoma.
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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.