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Epigenetic reprogramming through KDM6B drives immunofibroblast early commitment and immune properties

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE180245 | GEO | 2023/10/23

REPOSITORIES: GEO

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Epigenetic reprogramming through KDM6B drives immunofibroblast early commitment and immune properties [Mus_stromal_cells]

Project description:TLS are composed of immune cells, including lymphocytes and myeloid cells, lymphatic and blood endothelial cells, and PDPN+ stromal cells with lymphoid stromal cells (LSC) features called immunofibroblasts. These LSC play a central role in the physiology of secondary lymphoid organs. Recent studies have focused on the heterogeneity of immunofibroblast and their cell of origin, but molecular and epigenetic mechanisms involved in their commitment are still unknown. In this study, we took advantage of the combination of an in vitro model of human ASC commitment to LSC/immunofibroblasts, and an in vivo model of murine TLS induction. We highlighted in both cases an early induction of KDM6B in stromal cells associated with an early epigenetic reprogramming. The KDM6B signature was enriched in sorted pathogenic stroma from patients with autoimmune diseases. Furthermore, using a KDM6 inhibitor, we demonstrated that KDM6B was required for the acquisition of immunofibroblast phenotype and functions, including upregulation of CCL2 production and monocyte recruitment. Overall, our results shed light on epigenetic mechanisms involved in the early commitment, but also immune properties of immunofibroblasts.

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KDM6B drives epigenetic reprogramming associated with lymphoid stromal cell early commitment and immune properties.

Project description:Mature lymphoid stromal cells (LSCs) are key organizers of immune responses within secondary lymphoid organs. Similarly, inflammation-driven tertiary lymphoid structures depend on immunofibroblasts producing lymphoid cytokines and chemokines. Recent studies have explored the origin and heterogeneity of LSC/immunofibroblasts, yet the molecular and epigenetic mechanisms involved in their commitment are still unknown. This study explored the transcriptomic and epigenetic reprogramming underlying LSC/immunofibroblast commitment. We identified the induction of lysine demethylase 6B (KDM6B) as the primary epigenetic driver of early immunofibroblast differentiation. In addition, we observed an enrichment for KDM6B gene signature in murine inflammatory fibroblasts and pathogenic stroma of patients with autoimmune diseases. Last, KDM6B was required for the acquisition of LSC/immunofibroblast functional properties, including the up-regulation of CCL2 and the resulting recruitment of monocytes. Overall, our results reveal epigenetic mechanisms that participate in the early commitment and immune properties of immunofibroblasts and support the use of epigenetic modifiers as fibroblast-targeting strategies in chronic inflammation.

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Epigenetic reprogramming through KDM6B drives immunofibroblast early commitment and immune properties

Project description:Epigenetic reprogramming through KDM6B drives immunofibroblast early commitment and immune properties

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Project description:Epigenetic reprogramming through KDM6B drives immunofibroblast early commitment and immune properties [Hum_ASC_GSKJ4]