Does the PI3K pathway promote or antagonize regulatory T cell development and function?

被引：36

作者：

Soond, Dalya R. ^{[1
]}

Slack, Elizabeth C. M. ^{[1
,2
]}

Garden, Oliver A. ^{[2
]}

Patton, Daniel T. ^{[3
]}

Okkenhaug, Klaus ^{[1
]}

机构：

[1] Babraham Inst, Lab Lymphocyte Signalling & Dev, Cambridge CB22 3AT, England

[2] Univ London Royal Vet Coll, Dept Vet Clin Sci, Regulatory T Cell Lab Infect Immun Res Grp, London, England

[3] Univ British Columbia, Inst Life Sci, Dept Microbiol & Immunol, Vancouver, BC V5Z 1M9, Canada

来源：

FRONTIERS IN IMMUNOLOGY | 2012年 / 3卷

基金：

英国生物技术与生命科学研究理事会; 英国惠康基金;

关键词：

Akt; autoimmunity; Foxo; inflammation; mTOR; PI3K; T cell; Treg; PHOSPHOINOSITIDE 3-KINASE P110-DELTA; FOXP3; EXPRESSION; CUTTING EDGE; NEGATIVE REGULATION; P110-GAMMA ISOFORM; B-CELL; DIFFERENTIATION; INDUCTION; EFFECTOR; GENERATION;

D O I：

10.3389/fimmu.2012.00244

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Regulatory T cells (Tregs) prevent autoimmunity and nflammation by suppressing the activation of other T cells and antigen presenting cells. The role of phosphoinositide 3-kinase (PI3K) signaling in Treg is controversial. Some studies suggest that inhibition of the PI3K pathway is essential for the development of Tregs whereas other studies have shown reduced Treg numbers and function when PI3K activity is suppressed. Here we attempt to reconcile the different studies that have explored PI3K and the downstream effectors Akt, Foxo, and mTOR in regulatory T cell development and function and discuss the implications for health and therapeutic intervention.

引用

页数：8

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