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Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [ATAC-Seq]

ABSTRACT: We comapre mRNA expression level TOX and TOX2 CAR TILS and WT CAR TILs

ORGANISM(S): Mus musculus

PROVIDER: GSE130539 | GEO | 2019/05/31

REPOSITORIES: GEO

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Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [RNA-Seq]

Project description:We comapre mRNA expression level TOX and TOX2 CAR TILS and WT CAR TILs

2019-05-31 | GSE130538 | GEO

TOX2 coordinates with TET2 to positively regulate central memory differentiation in human CAR T cells

Project description:To investigate the effects of TOX and TOX2 on memory T cell differentiation in human CAR T cells, we used shRNA to knock down TOX2 or TOX, or overexpress FLAG-TOX2. We then performed gene expression profiling analysis using RNAseq, plus examined the binding of TOX2 to chromatin using ChIPseq.

2023-07-24 | GSE231620 | GEO

Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion

Project description:Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion

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Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [RNA-Seq]

Project description:Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [RNA-Seq]

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Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [ATAC-Seq]

Project description:Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion [ATAC-Seq]

| PRJNA540590 | ENA

TOX2 regulates human natural killer cell development by controlling T-BET expression

Project description:Thymocyte selection-associated high mobility group box protein family member 2 (TOX2) is a transcription factor belonging to the TOX family that shares a highly conserved high mobility group DNA binding domain with the other TOX members. While TOX1 has been shown to be an essential regulator of T-cell and natural killer (NK) cell differentiation in mice, little is known about the roles of the other TOX family members in lymphocyte development, particularly in humans. In this study, we found that TOX2 was preferentially expressed in mature human NK cells and was upregulated during in vitro differentiation of NK cells from human umbilical cord blood (UCB)M-bM-^@M-^Sderived CD34+ cells. Gene silencing of TOX2 intrinsically hindered the transition between early developmental stages of NK cells, while overexpression of TOX2 enhanced the development of mature NK cells from UCB CD34+ cells. We subsequently found that TOX2 was independent of ETS-1 but could directly upregulate the transcription of TBX21 (encoding T-BET). Overexpression of T-BET rescued the TOX2 knockdown phenotypes. Given the essential function of T-BET in NK cell differentiation, TOX2 therefore plays a crucial role in controlling normal NK cell development by acting upstream of TBX21 transcriptional regulation. survey of NK cells over time

2014-12-22 | E-GEOD-58589 | biostudies-arrayexpress

Distruption of TOX and TOX2 transcription factors in CAR T cells limits T cell exhaustion

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-31 | GSE130540 | GEO

TOX2 regulates human natural killer cell development by controlling T-BET expression

Project description:Thymocyte selection-associated high mobility group box protein family member 2 (TOX2) is a transcription factor belonging to the TOX family that shares a highly conserved high mobility group DNA binding domain with the other TOX members. While TOX1 has been shown to be an essential regulator of T-cell and natural killer (NK) cell differentiation in mice, little is known about the roles of the other TOX family members in lymphocyte development, particularly in humans. In this study, we found that TOX2 was preferentially expressed in mature human NK cells and was upregulated during in vitro differentiation of NK cells from human umbilical cord blood (UCB)–derived CD34+ cells. Gene silencing of TOX2 intrinsically hindered the transition between early developmental stages of NK cells, while overexpression of TOX2 enhanced the development of mature NK cells from UCB CD34+ cells. We subsequently found that TOX2 was independent of ETS-1 but could directly upregulate the transcription of TBX21 (encoding T-BET). Overexpression of T-BET rescued the TOX2 knockdown phenotypes. Given the essential function of T-BET in NK cell differentiation, TOX2 therefore plays a crucial role in controlling normal NK cell development by acting upstream of TBX21 transcriptional regulation.

2014-12-22 | GSE58589 | GEO

Genome binding/occupancy profiling of Tox2 in Tfh-like cells

Project description:T Follicular helper (Tfh) cell is an effector CD4+ T cell subset specialized in helping B cells in germinal centers (GC) reactions. Although Bcl6 was identified as a Tfh-specific transcription factor essential for their development, the molecular mechanisms underlying Bcl6 regulation and Tfh cell commitment remain unclear. Here, we report that Tox2 transcription factor is highly expressed in Tfh cells, regulated by Bcl6 and STAT3. Forced expression of Tox2 drives Bcl6 expression and Tfh development. Mechanistically, Tox2 directly binds to Tfh-associated genes, including Bcl6, and functions to promote their chromatin accessibility and modulate the activities of other Tfh-regulating factors. Conversely, genetic deletion of Tox2 results in defective Tfh differentiation, and inhibiting both Tox and Tox2 in T cells abolishes Tfh differentiation and GC response. Thus, our results demonstrate that Tox2 is a key transcription factor that regulates Bcl6 expression and Tfh development and suggest a Tox2-Bcl6 axis in feed-forward regulation of Tfh program.

2019-10-30 | GSE136539 | GEO

BATF and IRF4 cooperate to counter exhaustion in tumour-infiltrating CAR T cells (RNA-seq)

Project description:Cooperative interactions among transcription factors are essential for gene transcription. We previously showed that NFAT and AP-1 (Fos-Jun) transcription factors cooperate to promote the effector functions of T cells, but that under conditions where it is unable to cooperate with AP-1, NFAT imposes a negative feedback programme of T cell hyporesponsiveness (“exhaustion”). Here we show that BATF and IRF4 cooperate to counter T cell exhaustion. Overexpression of Batf in CD8+ 42 T cells expressing a chimeric antigen receptor (CAR) promoted the survival and expansion of tumour-infiltrating CAR T cells, increased their production of effector cytokines, decreased their expression of inhibitory receptors and the exhaustion-associated transcription factor TOX, and led to the generation of long-lived memory T cells that controlled tumour recurrence. These responses were dependent on the BATF-IRF interaction, since cells expressing a Batf mutant unable to interact with Irf4 did not survive in tumours and did not effectively delay tumour growth. We suggest that BATF overexpression is a therapeutically viable option for improving the anti-tumour responses of CAR TILs, by skewing their phenotypes and transcriptional profiles away from exhaustion and towards increased effector function.

2021-07-13 | GSE154745 | GEO

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