Chromatin accessibility of transcription factor Bach2 in mouse NK cells (ATAC-seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA877357 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21456888_1.fastq.gz | Fastqsanger.gz | |||
| SRR21456888_2.fastq.gz | Fastqsanger.gz | |||
| SRR21456889_1.fastq.gz | Fastqsanger.gz | |||
| SRR21456889_2.fastq.gz | Fastqsanger.gz | |||
| SRR21456890_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Transcription factor Bach2 has been reported to regulate the development and function of multiple immune cells including T cells and B cells. As a transcription repressor, Bach2 plays its role by repressing the expression of downstream targets. We are interested in whether Bach2 will affect NK cell development and what's the relationship between Bach2 and other transcription factors in regulating NK cell function. Here we try to explore the chromatin accessibility of Bach2 by ATAC-seq. We compared enriched peaks in mouse NK cell from Bach2 conditional knockout mice and control mice.
2022-09-07 | GSE212807 | GEO
Project description:Natural killer (NK) cells are critical to immune surveillance against infections and cancer. Their role in immune surveillance requires that NK cells are present within tissues in a quiescent state. Mechanisms by which NK cells remain quiescent in tissues are incompletely elucidated. The transcriptional repressor BACH2 plays a critical role within the adaptive immune system, but its function within innate lymphocytes has been unclear. Here, we show that BACH2 acts as an intrinsic negative regulator of NK cell maturation and function. BACH2 is expressed within developing and mature NK cells and promotes the maintenance of immature NK cells by restricting their maturation in the presence of weak stimulatory signals. Loss of BACH2 within NK cells results in accumulation of activated NK cells with unrestrained cytotoxic function within tissues, which mediate augmented immune surveillance to pulmonary cancer metastasis. These findings establish a critical function of BACH2 as a global negative regulator of innate cytotoxic function and tumor immune surveillance by NK cells.
2022-09-27 | GSE214128 | GEO
Project description:Bach2 has been reported to regulate multiple immune cell development and function. Here we report that Bach2 is constitutively expressed in relatively immature NK subsets. Bach2 negatively regulates NK cell development and Bach2 deficiency results in NK cell with mature effector phenotype. Thus, Bach2 functions as a negative regulator of NK cell maturation and function.
2022-02-10 | GSE196530 | GEO
Project description:To explore whether IRF4 deficiency determine the epigenetic changes of mature NK cells is at the NKP cell stage, ATAC-seq was performed to analyze chromatin accessibility of NK cells from spleen WT, Irf4-/-, Irf4flox/flox and Ncr1cre+/-Irf4flox/flox mice.
2024-12-11 | GSE283690 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE126806 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE137246 | GEO
Project description:ATAC-seq was performed on peripheral blood NK cells that were CRISPR-edited to knock-out expression of T-BET and EOMES. The following samples were analyzed to elucidate the role of T-BET and EOMES in regulating mature human NK cell chromatin accessibility.
2023-06-06 | GSE227878 | GEO
Project description:Through a diversity of functional lineages, cells of the innate and adaptive immune system either drive or constrain immune reactions within tumors. Thus, while the immune system has a powerful ability to recognize and kill cancer cells, this function is often suppressed preventing clearance of disease. The transcription factor (TF) BACH2 controls the differentiation and function of multiple innate and adaptive immune lineages, but its role in regulating tumor immunity is not known. Here, we demonstrate that BACH2 is required to establish immunosuppression within tumors. We found that growth of subcutaneously implanted tumors was markedly impaired in Bach2-deficient mice and coincided with intratumoral activation of both innate and adaptive immunity but was dependent upon adaptive immunity. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-γ. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression. These findings demonstrate that BACH2 is a key component of the molecular programme of tumor immunosuppression and identify a new target for development of therapies aimed at reversing immunosuppression in cancer. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-γ. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression.
2016-06-01 | E-GEOD-74653 | biostudies-arrayexpress
Project description:Through a diversity of functional lineages, cells of the innate and adaptive immune system either drive or constrain immune reactions within tumors. Thus, while the immune system has a powerful ability to recognize and kill cancer cells, this function is often suppressed preventing clearance of disease. The transcription factor (TF) BACH2 controls the differentiation and function of multiple innate and adaptive immune lineages, but its role in regulating tumor immunity is not known. Here, we demonstrate that BACH2 is required to establish immunosuppression within tumors. We found that growth of subcutaneously implanted tumors was markedly impaired in Bach2-deficient mice and coincided with intratumoral activation of both innate and adaptive immunity but was dependent upon adaptive immunity. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-γ. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression. These findings demonstrate that BACH2 is a key component of the molecular programme of tumor immunosuppression and identify a new target for development of therapies aimed at reversing immunosuppression in cancer.
2016-06-01 | GSE74653 | GEO
Project description:The differentiation and homeostasis of Foxp3+ regulatory T (Treg) cells is strictly controlled by T cell receptor (TCR) signals; however, the molecular regulators of these processes are incompletely known. Here we found that Bach2 was a key regulator of Treg cell differentiation and homeostasis downstream of TCR signalling. Bach2 prevented premature differentiation of fully suppressive effector (e)Treg cells, limited IL-10 production and was required for the development of peripherally induced (p)Treg cells in the gastrointestinal tract. We found that Bach2 attenuated TCR signalling-induced and IRF4-dependent Treg cell differentiation programs. Deletion of IRF4 promoted inducible Treg cell differentiation and rescued pTreg cell differentiation in the absence of Bach2. In turn, loss of Bach2 normalised eTreg cell differentiation of IRF4-deficient Treg cells. Mechanistically, Bach2 counteracted DNA-binding activity of IRF4 and limited chromatin accessibility, thereby attenuating IRF4-dependent transcriptional programs. Thus, Bach2 balanced TCR signalling induced transcriptional activity of IRF4 to maintain Treg cell homeostasis.
2019-11-07 | GSE126810 | GEO