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Bulk RNA-seq to study features of the transcriptome and TCR repertoire of a stably persisting population of regulatory T cells generated in mice with autoimmune inflammation by conversion from Treg "wannabes"

ABSTRACT: The immunosuppressive function of regulatory T (Treg) cells is dependent on continuous expression of the transcription factor Foxp3. Foxp3 loss-of-function or induced ablation of Treg cells results in a fatal autoimmune disease featuring all known types of inflammatory responses with every manifestation stemming from Treg cell paucity, highlighting a vital function of Treg cells in preventing fatal autoimmune inflammation. However, a major question remains whether Treg cells can persist and effectively exert their function in a disease state, where a broad spectrum of inflammatory mediators can either inactivate Treg cells or render innate and adaptive pro-inflammatory effector cells insensitive to suppression. By reinstating Foxp3 protein expression and suppressor function in cells expressing a reversible Foxp3 null allele in severely diseased mice, we found that the resulting single pool of “redeemed” Treg cells normalized immune activation, quelled severe tissue inflammation, reversed fatal autoimmune disease, and provided long-term protection against them. Thus, Treg cells are functional in settings of established broad spectrum systemic inflammation and are capable of affording sustained reset of immune homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE179706 | GEO | 2021/07/09

REPOSITORIES: GEO

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TCR-seq to study features of the transcriptome and TCR repertoire of a stably persisting population of regulatory T cells generated in mice with autoimmune inflammation by conversion from Treg "wannabes"

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Two Histone/Protein Acetyltransferases, CBP and p300, Are Indispensable for Foxp3+ T-regulatory Cell Development and Function

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Nemo-like kinase drives Foxp3 stability and is critical for maintenance of immune tolerance by regulatory T cells

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