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Mitochondrial and cytosolic roles of PINK1 shape induced regulatory T-cell development and function.

Abstract：

:Mutations in PTEN-induced kinase 1 (PINK1), a serine/threonine kinase linked to familial early-onset Parkinsonism, compromise mitochondrial integrity and metabolism and impair AKT signaling. As the activation of a naïve T cell requires an AKT-dependent reorganization of a cell's metabolic machinery, we sought to determine if PINK1-deficient T cells lack the ability to undergo activation and differentiation. We show that CD4(+) T cells from PINK1 knockout mice fail to properly phosphorylate AKT upon activation, resulting in reduced expression of the IL-2 receptor subunit CD25. Following, deficient IL-2 signaling mutes the activation-induced increase in respiratory capacity and mitochondrial membrane potential. Under polarization conditions favoring the development of induced regulatory T cells, PINK1(-/-) T cells exhibit a reduced ability to suppress bystander T-cell proliferation despite normal FoxP3 expression kinetics. Our results describe a critical role for PINK1 in integrating extracellular signals with metabolic state during T-cell fate determination, and may have implications for the understanding of altered T-cell populations and immunity during the progression of active Parkinson's disease or other immunopathologies.

journal_name

Eur J Immunol

journal_title

European journal of immunology

authors

Ellis GI,Zhi L,Akundi R,Büeler H,Marti F

doi

10.1002/eji.201343571

subject

Has Abstract

pub_date

2013-12-01 00:00:00

pages

3355-60

issue

12

eissn

0014-2980

issn

1521-4141

journal_volume

43

pub_type

杂志文章

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