Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced TOU

Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced
 TOU

Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced

Abstract

Steroid nuclear receptor coactivator 2 (SRC2) is a member of a family of transcription coactivators. While SRC1 inhibits the differentiation of regulatory T cells (T

regs

) critical for establishing immune tolerance, we show here that SRC2 stimulates T

reg

differentiation. SRC2 is dispensable for the development of thymic T

regs

whereas naive CD4

+

T cells from mice deficient of SRC2 specific in T

regs

(

SRC2

fl / fl

/ Foxp3

YFP-Cre

) display defective T

reg

differentiation. Furthermore, the aged

SRC2

fl / fl

/ Foxp3

YFP-Cre

mice spontaneously develop autoimmune phenotypes including enlarged spleen and lung inflammation infiltrated with IFNγ-producing CD4

+

T cells.

SRC2

fl / fl

/ Foxp3

YFP-Cre

mice also develop severer experimental autoimmune encephalomyelitis (EAE) due to reduced T

regs

. Mechanically, SRC2 recruited by NFAT1 binds to the promoter and activates the expression of

Nr4a2

which then stimulates Foxp3 expression to promote T

reg

differentiation. Members of SRC family coactivators thus play distinct roles in T

reg

differentiation and are potential drug targets for controlling immune tolerance.

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