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In situ conversion of defective Treg into SuperTreg cells to treat advanced IPEX-like disorders in mice.

Abstract：

:Mutations disrupting regulatory T (Treg) cell function can cause IPEX and IPEX-related disorders, but whether established disease can be reversed by correcting these mutations is unclear. Treg-specific deletion of the chromatin remodeling factor Brg1 impairs Treg cell activation and causes fatal autoimmunity in mice. Here, we show with a reversible knockout model that re-expression of Brg1, in conjunction with the severe endogenous proinflammatory environment, can convert defective Treg cells into powerful, super-activated Treg cells (SuperTreg cells) that can resolve advanced autoimmunity,  with  Brg1 re-expression in a minor fraction of Treg cells sufficient for the resolution in some cases. SuperTreg cells have enhanced trafficking and regulatory capabilities, but become deactivated as the inflammation subsides, thus avoiding excessive immune suppression. We propose a simple, robust yet safe gene-editing-based therapy for IPEX and IPEX-related disorders that exploits the defective Treg cells and the inflammatory environment pre-existing in the patients.

journal_name

Nat Commun

journal_title

Nature communications

authors

Li Y,Chen Y,Mao S,Kaundal R,Jing Z,Chen Q,Wang X,Xia J,Liu D,Sun J,Wang H,Chi T

doi

10.1038/s41467-020-15836-2

subject

Has Abstract

pub_date

2020-06-03 00:00:00

pages

2781

issue

1

issn

2041-1723

pii

10.1038/s41467-020-15836-2

journal_volume

11

pub_type

杂志文章

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