BLIMP1 negatively regulates IL-2 signaling in T cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1112429 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29060631.fastq.gz | Fastqsanger.gz | |||
| SRR29060632.fastq.gz | Fastqsanger.gz | |||
| SRR29060633.fastq.gz | Fastqsanger.gz | |||
| SRR29060634.fastq.gz | Fastqsanger.gz | |||
| SRR29060635.fastq.gz | Fastqsanger.gz |
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Project description:BLIMP1 negatively regulates IL-2 signaling in T cells
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Project description:IL-2 signaling sustains immune homeostasis by fine-tuning the balance between effector and regulatory T cells. Our genome-wide CRISPR knockout screen using IL-2-dependent cells derived from a patient with Adult T-cell Leukemia (ATL) showed enriched sgRNAs targeting PRDM1 (encoding BLIMP1). BLIMP1 inhibits IL-2 production in T cells; however, its role in IL-2 signaling remains unknown. Here, we show that Prdm1 overexpression decreased IL-2 signaling in CD4+ T cells, while its deletion enhanced IL-2 signaling during influenza infection. Adoptive transfer of Prdm1 CKO Tregs into Rag2-/- mice elevated IL-2 signaling in T-cell induced colitis. Moreover, CRISPR/Cas9-mediated PRDM1 deletion augmented IL-2 signaling in human CD4+ T cells and natural Tregs with BLIMP1 binding to key genes affecting IL-2 signaling. Furthermore, ATL cells from acute patients exhibited increased IL-2 signaling but reduced BLIMP1 induction. Thus, BLIMP1 represses IL-2 signaling in T cells which is critical in orchestrating normal and pathophysiological immune responses.
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Project description:IL-2 signaling sustains immune homeostasis by fine-tuning the balance between effector and regulatory T cells. Our genome-wide CRISPR knockout screen using IL-2-dependent cells derived from a patient with Adult T-cell Leukemia (ATL) showed enriched sgRNAs targeting PRDM1 (encoding BLIMP1). BLIMP1 inhibits IL-2 production in T cells; however, its role in IL-2 signaling remains unknown. Here, we show that Prdm1 overexpression decreased IL-2 signaling in CD4+ T cells, while its deletion enhanced IL-2 signaling during influenza infection. Adoptive transfer of Prdm1 CKO Tregs into Rag2-/- mice elevated IL-2 signaling in T-cell induced colitis. Moreover, CRISPR/Cas9-mediated PRDM1 deletion augmented IL-2 signaling in human CD4+ T cells and natural Tregs with BLIMP1 binding to key genes affecting IL-2 signaling. Furthermore, ATL cells from acute patients exhibited increased IL-2 signaling but reduced BLIMP1 induction. Thus, BLIMP1 represses IL-2 signaling in T cells which is critical in orchestrating normal and pathophysiological immune responses.
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Project description:IL-2 signaling sustains immune homeostasis by fine-tuning the balance between effector and regulatory T cells. Our genome-wide CRISPR knockout screen using IL-2-dependent cells derived from a patient with Adult T-cell Leukemia (ATL) showed enriched sgRNAs targeting PRDM1 (encoding BLIMP1). BLIMP1 inhibits IL-2 production in T cells; however, its role in IL-2 signaling remains unknown. Here, we show that Prdm1 overexpression decreased IL-2 signaling in CD4+ T cells, while its deletion enhanced IL-2 signaling during influenza infection. Adoptive transfer of Prdm1 CKO Tregs into Rag2-/- mice elevated IL-2 signaling in T-cell induced colitis. Moreover, CRISPR/Cas9-mediated PRDM1 deletion augmented IL-2 signaling in human CD4+ T cells and natural Tregs with BLIMP1 binding to key genes affecting IL-2 signaling. Furthermore, ATL cells from acute patients exhibited increased IL-2 signaling but reduced BLIMP1 induction. Thus, BLIMP1 represses IL-2 signaling in T cells which is critical in orchestrating normal and pathophysiological immune responses.
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Project description:IL-2 signaling sustains immune homeostasis by fine-tuning the balance between effector and regulatory T cells. Our genome-wide CRISPR knockout screen using IL-2-dependent cells derived from a patient with Adult T-cell Leukemia (ATL) showed enriched sgRNAs targeting PRDM1 (encoding BLIMP1). BLIMP1 inhibits IL-2 production in T cells; however, its role in IL-2 signaling remains unknown. Here, we show that Prdm1 overexpression decreased IL-2 signaling in CD4+ T cells, while its deletion enhanced IL-2 signaling during influenza infection. Adoptive transfer of Prdm1 CKO Tregs into Rag2-/- mice elevated IL-2 signaling in T-cell induced colitis. Moreover, CRISPR/Cas9-mediated PRDM1 deletion augmented IL-2 signaling in human CD4+ T cells and natural Tregs with BLIMP1 binding to key genes affecting IL-2 signaling. Furthermore, ATL cells from acute patients exhibited increased IL-2 signaling but reduced BLIMP1 induction. Thus, BLIMP1 represses IL-2 signaling in T cells which is critical in orchestrating normal and pathophysiological immune responses.
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Project description:Distinct metabolic programs support the differentiation of CD4+T cells into their separate lineages. In this study, we investigated metabolic mechanisms underlying the differentiation of IL-9 producing-CD4+T cells (TH9) in allergic airway inflammation and cancerous tumors. We found here that SIRT1 negatively regulates TH9 differentiation. A deficiency of SIRT1 induced by either conditional deletion in mouse CD4+T cells or the use of small interfering RNA (siRNA) in mouse or human T cells increased IL-9 production, whereas ectopic SIRT1 expression inhibited it. Notably, SIRT1-inhibited the differentiation of TH9 cells that regulated anti-tumor immunity and allergic pulmonary inflammation. Glycolytic activation through the mTOR-hypoxia-inducible factor-1α (HIF1α) pathway was required for the differentiation of the TH9 cells that confer protection against tumors and are involved in allergic airway inflammation. Our results define the essential features of a SIRT1-mTOR-HIF1α signaling-coupled glycolytic pathway in inducing TH9 cell differentiation, with implications for metabolic reprogramming as an immunotherapeutic approach. Lymphocytes were isolated from the spleen and lymph nodes of mice and sorted on a FACSAria II (Becton Dickinson). The sorted naïve T cells (CD4+TCR+CD62Lhi CD44lo) from WT or SIRT1flox/flox-CD4-Cre mice were used for in vitro culture. T cells were activated with 2 ug/ml anti-CD3 (2C11; Bio X Cell), 2 ug/ml anti-CD28 (37.51; Bio X Cell) and 100 U/ml human IL-2. For TH9 cell differentiation, cultures were supplemented with 10 ng/ml IL-4 (R&D system), 2 ng/ml TGFβ1 (R&D system). After 5-6 d culture, differentiated T cells were collected and for microarray assay.
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