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Extracellular traps released by antimicrobial TH17 cells contributes to host defense

ABSTRACT: Extracellular traps released by antimicrobial TH17 cells contributes to host defense

PROVIDER: PRJNA605152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11034850.fastq.gz	Fastqsanger.gz
	SRR11034851.fastq.gz	Fastqsanger.gz
	SRR11034852.fastq.gz	Fastqsanger.gz
	SRR11034853.fastq.gz	Fastqsanger.gz
	SRR11034854.fastq.gz	Fastqsanger.gz

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Extracellular traps released by antimicrobial TH17 cells contributes to host defense

Project description:Herein, we used C. acnes as a model to elucidate the antimicrobial machinery of the TH17 subset. We generated C. acnes-specific antimicrobial TH17 clones (AMTH17) with varying antimicrobial activity against C. acnes, to enable us to study mechanisms by which TH17 cells kill bacteria. We show that C. acnes-induced AMTH17 clones represent a subset of CD4+ TEM and TEMRA cells. RNA-seq analysis of AMTH17 indicate transcripts encoding antimicrobial molecules such as GNLY, GZMB, PRF1 and histone H2B, whose expression correlates with killing activity. Additionally, we validated that AMTH17-mediated killing is a general mechanism that can target C. acnes and other bacterial species. Scanning electron microscopy reveal that AMTH17s can release T cell extracellular traps composed of lysine and arginine-rich histones such as H2B and H4 that entangle C. acnes. This study identifies a functionally distinct subpopulation of TH17 cells with an ability to secrete antimicrobial proteins and form extracellular T cell traps to capture and kill bacteria.

2021-12-01 | GSE144852 | GEO

Extracellular traps released by antimicrobial TH17 cells contribute to host defense.

Project description:TH17 cell subpopulations have been defined that contribute to inflammation and homeostasis, yet the characteristics of TH17 cells that contribute to host defense against infection are not clear. To elucidate the antimicrobial machinery of the TH17 subset, we studied the response to Cutibacterium acnes, a skin commensal that is resistant to IL-26, the only known TH17-secreted protein with direct antimicrobial activity. We generated C. acnes-specific antimicrobial TH17 clones (AMTH17) with varying antimicrobial activity against C. acnes, which we correlated by RNA sequencing to the expression of transcripts encoding proteins that contribute to antimicrobial activity. Additionally, we validated that AMTH17-mediated killing of C. acnes and bacterial pathogens was dependent on the secretion of granulysin, granzyme B, perforin, and histone H2B. We found that AMTH17 cells can release fibrous structures composed of DNA decorated with histone H2B that entangle C. acnes that we call T cell extracellular traps (TETs). Within acne lesions, H2B and IL-17 colocalized in CD4+ T cells, in proximity to TETs in the extracellular space composed of DNA decorated with H2B. This study identifies a functionally distinct subpopulation of TH17 cells with an ability to form TETs containing secreted antimicrobial proteins that capture and kill bacteria.

| S-EPMC7810473 | biostudies-literature

BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

Project description:CD4+ T helper 17 (Th17) cells protect vertebrate hosts from extracellular pathogens at mucosal surfaces. Th17 cells form from naïve precursors when signals from the T cell antigen receptor (TCR) and certain cytokine receptors induce the expression of the RORγt transcription factor, which activates a set of Th17-specific genes. Using T cell-specific loss-of-function experiments we find that two components of the Polycomb Repressive Complex 1.1 (PRC1.1), BCL6 corepressor (BCOR) and KDM2B, which helps target the complex to unmethylated CpG DNA islands, are required for optimal Th17 cell formation in mice after Streptococcus pyogenes infection. Genome-wide expression and BCOR chromatin immunoprecipitation studies revealed that BCOR directly represses Lef1, Runx2, and Dusp4, whose products inhibit Th17 differentiation. Together, the results suggest that PRC1.1 components, BCOR and KDM2B, work together to enhance Th17 cell formation by repressing Th17 fate suppressors.

2019-04-26 | GSE121766 | GEO

CIP2A negatively regulates Th17 differentiation

Project description:Interleukin 17 (IL-17) producing T helper 17 (Th17) cells are critical drivers of pathogenesis in a variety of autoimmune and inflammatory diseases. Strategies to mitigate excessive Th17 response thus remain an attractive target for immunotherapies. Here we report that Cancerous Inhibitor of Protein Phosphatase 2A (CIP2A) regulates IL-17 production by Th17 cells in human and mouse. Using CIP2A knock-out (KO) mice and siRNA-mediated CIP2A silencing in human primary CD4+ T cells, we demonstrated that CIP2A silencing results in a significant increase in IL-17 production. Interestingly, CIP2A deficient Th17 cells were characterized by increased strength and duration of STAT3 (Y705) phosphorylation. Genome-wide gene expression profile as well as the p-STAT3 (Y705) interactome of CIP2A deficient Th17 cells identified that CIP2A regulates the strength of the interaction between Acylglycerol kinase (AGK) and STAT3, and thereby, modulates STAT3 phosphorylation as well as expression of IL-17 in Th17 cells. Our results uncover the physiological function of CIP2A in Th17 cells and provides new opportunities for therapeutic intervention in Th17 cell mediated diseases.

2020-05-26 | PXD010612 | Pride

Innate immunity turned inside-out: antimicrobial defense by phagocyte extracellular traps.

Project description:The formation of extracellular traps (ETs) by phagocytic cells has been recognized as a novel and important mechanism of the host innate immune response against infections. ETs are formed by different host immune cells such as neutrophils, mast cells, and eosinophils after stimulation with mitogens, cytokines, or pathogens themselves, in a process dependent upon induction of a reactive-oxygen-species-mediated signaling cascade. ETs consist of nuclear or mitochondrial DNA as a backbone with embedded antimicrobial peptides, histones, and cell-specific proteases and thereby provide a matrix to entrap and kill microbes and to induce the contact system. This review summarizes the latest research on ETs and their role in innate immunity and host innate defense. Attention is also given to mechanisms by which certain leading bacterial pathogens have evolved to avoid entrapment and killing in these specialized structures.

| S-EPMC2707954 | biostudies-other

Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

Project description:This SuperSeries is composed of the following subset Series: GSE32542: Murine serum reactivity to common autoantigens in response to immunization with neutrophil extracellular traps GSE32543: Human and murine serum reactivity to specific histone posttranslational modifications in neutrophil extracellular traps Refer to individual Series

2012-01-26 | E-GEOD-32544 | biostudies-arrayexpress

Long Intergenic Noncoding RNA MIAT Contributes to Human Th17 Cell Differentiation

Project description:T helper 17 (Th17) cells protect against fungal and bacterial infections and are implicated in autoimmunity. Several long intergenic noncoding RNAs (lincRNA) are induced during Th17 differentiation, however, their contribution to Th17 differentiation is poorly understood. We discovered a lincRNA myocardial infarction associated transcript (MIAT) to be upregulated early after induction of human Th17 cell differentiation along with an increase in the chromatin accessibility at the gene locus. RNA-seq analysis identified genes implicated in Th17 differentiation and functions as MIAT targets. Our data suggests that MIAT contributes to human Th17 differentiation by upregulating several genes implicated in Th17 differentiation.

2022-05-25 | GSE183664 | GEO

Human Th17 Cell differentiation

Project description:The early stages of human Th17 Cell differentiation were studied using label free proteomics to compare Th17 polarized CD4+ human T cells at 24 h and 72 h with activated cells (72 and 24 h) and Thp cells.

2019-01-28 | PXD008973 | Pride

Effect of Neutrophil Extracellular Traps and Psoriasis-Associated TRAF3IP2 Genotype on Induction of Human Th17 Cells

Project description:Effect of Neutrophil Extracellular Traps and Psoriasis-Associated TRAF3IP2 Genotype on Induction of Human Th17 Cells

| PRJNA497059 | ENA

BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

Project description:BCL6 corepressor contributes to Th17 cell formation by inhibiting Th17 fate suppressors

| PRJNA498403 | ENA