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Times Cited: 252
Times Cited
Times Co-cited
Similarity
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Follicular CXCR5- expressing CD8(+) T cells curtail chronic viral infection.
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T Cell Factor 1-Expressing Memory-like CD8(+) T Cells Sustain the Immune Response to Chronic Viral Infections.
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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Subsets of exhausted CD8+ T cells differentially mediate tumor control and respond to checkpoint blockade.
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The TCF1-Bcl6 axis counteracts type I interferon to repress exhaustion and maintain T cell stemness.
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Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection.
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TOX reinforces the phenotype and longevity of exhausted T cells in chronic viral infection.
Francesca Alfei, Kristiyan Kanev, Maike Hofmann, Ming Wu, Hazem E Ghoneim, Patrick Roelli, Daniel T Utzschneider, Madlaina von Hoesslin, Jolie G Cullen, Yiping Fan,[...]. Nature 2019
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TOX transcriptionally and epigenetically programs CD8+ T cell exhaustion.
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High-dimensional single cell analysis identifies stem-like cytotoxic CD8+ T cells infiltrating human tumors.
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TOX is a critical regulator of tumour-specific T cell differentiation.
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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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Epigenetic stability of exhausted T cells limits durability of reinvigoration by PD-1 blockade.
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TCF-1-Centered Transcriptional Network Drives an Effector versus Exhausted CD8 T Cell-Fate Decision.
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TOX and TOX2 transcription factors cooperate with NR4A transcription factors to impose CD8+ T cell exhaustion.
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Inflammation directs memory precursor and short-lived effector CD8(+) T cell fates via the graded expression of T-bet transcription factor.
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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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Molecular and cellular insights into T cell exhaustion.
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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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Checkpoint Blockade Immunotherapy Induces Dynamic Changes in PD-1-CD8+ Tumor-Infiltrating T Cells.
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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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Chromatin states define tumour-specific T cell dysfunction and reprogramming.
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Essential role of the Wnt pathway effector Tcf-1 for the establishment of functional CD8 T cell memory.
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CXCR5+ CCR7- CD8 T cells are early effector memory cells that infiltrate tonsil B cell follicles.
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Dynamics of SIV-specific CXCR5+ CD8 T cells during chronic SIV 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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Effector and memory CD8+ T cell fate coupled by T-bet and eomesodermin.
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Molecular signature of CD8+ T cell exhaustion during chronic viral infection.
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The transcription factor NFAT promotes exhaustion of activated CD8⁺ T cells.
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Dysfunctional CD8 T Cells Form a Proliferative, Dynamically Regulated Compartment within Human Melanoma.
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Precursor exhausted T cells: key to successful immunotherapy?
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Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of T follicular helper cell differentiation.
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Viral persistence alters CD8 T-cell immunodominance and tissue distribution and results in distinct stages of functional impairment.
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Restoring function in exhausted CD8 T cells during chronic viral infection.
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An intra-tumoral niche maintains and differentiates stem-like CD8 T cells.
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Early precursor T cells establish and propagate T cell exhaustion in chronic infection.
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Control of effector CD8+ T cell function by the transcription factor Eomesodermin.
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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.