Metabolic regulation of organelle homeostasis in lupus T cells

被引：53

作者：

Caza, Tiffany N.

Talaber, Gergely

Perl, Andras ^{[1
]}

机构：

[1] SUNY Upstate Med Univ, Div Rheunnatol, Dept Med, Syracuse, NY 13210 USA

来源：

CLINICAL IMMUNOLOGY | 2012年 / 144卷 / 03期

关键词：

Systemic lupus erythematosus; T cell; Mitochondria; Endocytic recycling; Mammalian target of rapamycin; Autophagy; AUTOIMMUNE KIDNEY-DISEASE; RECEPTOR ZETA-CHAIN; RAPAMYCIN COMPLEX 1; SYSTEMIC-LUPUS; MAMMALIAN TARGET; MITOCHONDRIAL HYPERPOLARIZATION; MONOCLONAL-ANTIBODY; NITRIC-OXIDE; IMMUNOLOGICAL SYNAPSE; B-LYMPHOCYTE;

D O I：

10.1016/j.clim.2012.07.001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Abnormal T-cell signaling and activation are characteristic features in systemic lupus erythematosus (SLE). Lupus T cells are shifted toward an over-activated state, important signaling pathways are rewired, and signaling molecules are replaced. Disturbances in metabolic and organelle homeostasis, importantly within the mitochondrial, endosomal, and autophagosomal compartments, underlie the changes in signal transduction. Mitochondrial hyperpolarization, enhanced endosomal recycling, and dysregulated autophagy are hallmarks of pathologic organelle homeostasis in SLE. This review is focused on the metabolic checkpoints of endosomal traffic that control immunological synapse formation and mitophagy and may thus serve as targets for treatment in SLE. (c) 2012 Elsevier Inc. All rights reserved.

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收藏

页码：200 / 213

页数：14

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