The PI3K pathway in B cell metabolism

被引：118

作者：

Jellusova, Julia ^{[1
,2
]}

Rickert, Robert C. ^{[3
]}

机构：

[1] Albert Ludwigs Univ Freiburg, BIOSS Ctr Biol Signalling Studies, Freiburg, Germany

[2] Max Planck Inst Immunobiol & Epigenet, Freiburg, Germany

[3] Sanford Burnham Prebys Med Discovery Inst, 10901 N Torrey Pines Rd, La Jolla, CA 92037 USA

来源：

CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY | 2016年 / 51卷 / 05期

基金：

美国国家卫生研究院;

关键词：

Akt; mTOR; lymphocyte; glycolysis; mitochondria; GLYCOGEN-SYNTHASE KINASE-3; PHOSPHOINOSITIDE 3-KINASE P110-DELTA; ANTIGEN RECEPTOR ENGAGEMENT; CLASS-SWITCH RECOMBINATION; NF-KAPPA-B; GERMINAL CENTER; PHOSPHATIDYLINOSITOL; 3-KINASE; SIGNALING PATHWAY; GLUCOSE-METABOLISM; HYDROGEN-PEROXIDE;

D O I：

10.1080/10409238.2016.1215288

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

B cell growth and proliferation is tightly regulated by signaling through the B cell receptor and by other membrane bound receptors responding to different cytokines. The PI3K signaling pathway has been shown to play a crucial role in B cell activation, differentiation and survival. Activated B cells undergo metabolic reprograming in response to changing energetic and biosynthetic demands. B cells also need to be able to coordinate metabolic activity and proliferation with nutrient availability. The PI3K signaling network has been implicated in regulating nutrient acquisition, utilization and biosynthesis, thus integrating receptor-mediated signaling with cell metabolism. In this review, we discuss the current knowledge about metabolic changes induced in activated B cells, strategies to adapt to metabolic stress and the role of PI3K signaling in these processes.

引用

页码：359 / 378

页数：20

共 159 条

[1] αv Integrins combine with LC3 and atg5 to regulate Toll-like receptor signalling in B cells [J].

Acharya, Mridu ;

Sokolovska, Anna ;

Tam, Jenny M. ;

Conway, Kara L. ;

Stefani, Caroline ;

Raso, Fiona ;

Mukhopadhyay, Subhankar ;

Feliu, Marianela ;

Paul, Elahna ;

Savill, John ;

Hynes, Richard O. ;

Xavier, Ramnik J. ;

Vyas, Jatin M. ;

Stuart, Lynda M. ;

Lacy-Hulbert, Adam .

NATURE COMMUNICATIONS, 2016, 7

[2]

Ahn CS, 2015, CANCER METAB, V3, DOI 10.1186/s40170-015-0128-2

[3] Foxo1 directly regulates the transcription of recombination-activating genes during B cell development [J].

Amin, Rupesh H. ;

Schlissel, Mark S. .

NATURE IMMUNOLOGY, 2008, 9 (06) :613-622

[4] Pten inactivation alters peripheral B lymphocyte fate and reconstitutes CD19 function [J].

Anzelon, AN ;

Wu, H ;

Rickert, RC .

NATURE IMMUNOLOGY, 2003, 4 (03) :287-294

[5]

Argyriou Pinelopi, 2012, Adv Hematol, V2012, P435342, DOI 10.1155/2012/435342

[6] Autophagy is dispensable for B-cell development but essential for humoral autoimmune responses [J].

Arnold, J. ;

Murera, D. ;

Arbogast, F. ;

Fauny, J-D ;

Muller, S. ;

Gros, F. .

CELL DEATH AND DIFFERENTIATION, 2016, 23 (05) :853-864

[7] Emergence of the PI3-kinase pathway as a central modulator of normal and aberrant B cell differentiation [J].

Baracho, G. V. ;

Miletic, A. V. ;

Omori, S. A. ;

Cato, M. H. ;

Rickert, R. C. .

CURRENT OPINION IN IMMUNOLOGY, 2011, 23 (02) :178-183

[8] PDK1 regulates B cell differentiation and homeostasis [J].

Baracho, Gisele V. ;

Cato, Matthew H. ;

Zhu, Zilu ;

Jaren, Olav R. ;

Hobeika, Elias ;

Reth, Michael ;

Rickert, Robert C. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2014, 111 (26) :9573-9578

[9] Direct activation of mTOR in B lymphocytes confers impairment in B-cell maturation and loss of marginal zone B cells [J].

Benhamron, Sandrine ;

Tirosh, Boaz .

EUROPEAN JOURNAL OF IMMUNOLOGY, 2011, 41 (08) :2390-2396

[10] On the Redox Control of B Lymphocyte Differentiation and Function [J].

Bertolotti, Milena ;

Sitia, Roberto ;

Rubartelli, Anna .

ANTIOXIDANTS & REDOX SIGNALING, 2012, 16 (10) :1139-1149

← 1 2 3 4 5 6 7 8 9 10 →