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ICOS coreceptor signaling inactivates the transcription factor FOXO1 to promote Tfh cell differentiation.

Abstract：

:T follicular helper (Tfh) cells are essential in the induction of high-affinity, class-switched antibodies. The differentiation of Tfh cells is a multi-step process that depends upon the co-receptor ICOS and the activation of phosphoinositide-3 kinase leading to the expression of key Tfh cell genes. We report that ICOS signaling inactivates the transcription factor FOXO1, and a Foxo1 genetic deletion allowed for generation of Tfh cells with reduced dependence on ICOS ligand. Conversely, enforced nuclear localization of FOXO1 inhibited Tfh cell development even though ICOS was overexpressed. FOXO1 regulated Tfh cell differentiation through a broad program of gene expression exemplified by its negative regulation of Bcl6. Final differentiation to germinal center Tfh cells (GC-Tfh) was instead FOXO1 dependent as the Foxo1(-/-) GC-Tfh cell population was substantially reduced. We propose that ICOS signaling transiently inactivates FOXO1 to initiate a Tfh cell contingency that is completed in a FOXO1-dependent manner.

journal_name

Immunity

journal_title

Immunity

authors

Stone EL,Pepper M,Katayama CD,Kerdiles YM,Lai CY,Emslie E,Lin YC,Yang E,Goldrath AW,Li MO,Cantrell DA,Hedrick SM

doi

10.1016/j.immuni.2015.01.017

subject

Has Abstract

pub_date

2015-02-17 00:00:00

pages

239-251

issue

2

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(15)00043-6

journal_volume

42

pub_type

杂志文章

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