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Transcriptional signature of human pro-inflammatory TH17 cells

ABSTRACT: Transcriptional signature of human pro-inflammatory TH17 cells

PROVIDER: PRJNA407976 | ENA |

REPOSITORIES: ENA

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Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

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Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

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Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity

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Autoimmunity and infection give rise to distict inflammatory Th17 subsets [bulk RNA-seq]

Project description:Th17 cells are a heterogeneous population that is critical for tissue homeostasis and inflammation during clearance of infections and autoimmunity. Despite substantial efforts distinguishing homeostatic and inflammatory roles of Th17 cells, the mechanism underlying the divergent functions of inflammatory Th17 cells is poorly understood. In this study, we show that the inflammatory Th17 engaged in autoimmune colitis and those involved in infection-induced colitis are two distinguishable populations illustrated by their distinct responses to a pharmacological molecule, clofazimine (CLF). Distinct from existing Th17 inhibitors, CLF selectively inhibits pro-autoimmune Th17 cells while preserving the functional state of infection-elicited Th17 cells through restricting Aldh1l2expression. Using bulk RNA sequencing, we explored transcriptional response to CLF on in vitro differentiated inflammatory and homeostatic Th17 cells. Notably, we identified a unique suppression in the transcription of signature inflammatory genes in Th17 cells with a marginal effect on those elicited by infection.

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Autoimmunity and infection give rise to distict inflammatory Th17 subsets [single-cell RNA-seq]

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Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity I

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