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免疫相关肌动蛋白病揭示的T细胞突触处的肌动蛋白动力学

Actin Dynamics at the T Cell Synapse as Revealed by Immune-Related Actinopathies.

作者信息

Dupré Loïc, Boztug Kaan, Pfajfer Laurène

机构信息

Ludwig Boltzmann Institute for Rare and Undiagnosed Diseases (LBI-RUD), Vienna, Austria.

Department of Dermatology, Medical University of Vienna, Vienna, Austria.

出版信息

Front Cell Dev Biol. 2021 Jun 24;9:665519. doi: 10.3389/fcell.2021.665519. eCollection 2021.


DOI:10.3389/fcell.2021.665519
PMID:34249918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8266300/
Abstract

The actin cytoskeleton is composed of dynamic filament networks that build adaptable local architectures to sustain nearly all cellular activities in response to a myriad of stimuli. Although the function of numerous players that tune actin remodeling is known, the coordinated molecular orchestration of the actin cytoskeleton to guide cellular decisions is still ill defined. T lymphocytes provide a prototypical example of how a complex program of actin cytoskeleton remodeling sustains the spatio-temporal control of key cellular activities, namely antigen scanning and sensing, as well as polarized delivery of effector molecules, via the immunological synapse. We here review the unique knowledge on actin dynamics at the T lymphocyte synapse gained through the study of primary immunodeficiences caused by mutations in genes encoding actin regulatory proteins. Beyond the specific roles of individual actin remodelers, we further develop the view that these operate in a coordinated manner and are an integral part of multiple signaling pathways in T lymphocytes.

摘要

肌动蛋白细胞骨架由动态丝状网络组成,这些网络构建可适应的局部结构,以响应无数刺激维持几乎所有细胞活动。尽管已知许多调节肌动蛋白重塑的因子的功能,但肌动蛋白细胞骨架协调分子编排以指导细胞决策仍不清楚。T淋巴细胞提供了一个典型例子,说明肌动蛋白细胞骨架重塑的复杂程序如何通过免疫突触维持关键细胞活动的时空控制,即抗原扫描和感知,以及效应分子的极化递送。我们在此回顾通过研究由编码肌动蛋白调节蛋白的基因突变引起的原发性免疫缺陷而获得的关于T淋巴细胞突触处肌动蛋白动力学的独特知识。除了单个肌动蛋白重塑因子的特定作用外,我们进一步提出观点,即这些因子以协调方式运作,并且是T淋巴细胞中多个信号通路的组成部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/3f60511bc22b/fcell-09-665519-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/d70711932429/fcell-09-665519-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/0083d8580674/fcell-09-665519-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/3f60511bc22b/fcell-09-665519-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/d70711932429/fcell-09-665519-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/0083d8580674/fcell-09-665519-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a4f3/8266300/3f60511bc22b/fcell-09-665519-g003.jpg

相似文献

[1]
Actin Dynamics at the T Cell Synapse as Revealed by Immune-Related Actinopathies.

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[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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引用本文的文献

[1]
Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.

Nat Rev Immunol. 2025-9-10

[2]
β-Actin Deficiency in Baraitser-Winter Syndrome Type 1 Disrupts T-Cell Function and Immune Regulation: Implications for Targeted Therapy in Actinopathies.

J Clin Immunol. 2025-8-1

[3]
Hem1 controls T cell activation, memory, and the regulated release of immunosuppressive and proinflammatory cytokines.

JCI Insight. 2025-7-8

[4]
Mitochondrial Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.

Physiology (Bethesda). 2025-7-1

[5]
Accurate sequence-to-affinity models for SH2 domains from multi-round peptide binding assays coupled with free-energy regression.

bioRxiv. 2025-1-5

[6]
Bayesian metamodeling of early T-cell antigen receptor signaling accounts for its nanoscale activation patterns.

Front Immunol. 2024

[7]
Formin-like 1β phosphorylation at S1086 is necessary for secretory polarized traffic of exosomes at the immune synapse in Jurkat T lymphocytes.

Elife. 2024-10-31

[8]
DRAK2 regulates myosin light chain phosphorylation in T cells.

J Cell Sci. 2024-11-15

[9]
Novel FRET-based Immunological Synapse Biosensor for the Prediction of Chimeric Antigen Receptor-T Cell Function.

Small Methods. 2025-3

[10]
DIAPH1-Deficiency is Associated with Major T, NK and ILC Defects in Humans.

J Clin Immunol. 2024-8-9

本文引用的文献

[1]
Loss of DIAPH1 causes SCBMS, combined immunodeficiency, and mitochondrial dysfunction.

J Allergy Clin Immunol. 2021-8

[2]
RhoG deficiency abrogates cytotoxicity of human lymphocytes and causes hemophagocytic lymphohistiocytosis.

Blood. 2021-4-15

[3]
Coordinating Cytoskeleton and Molecular Traffic in T Cell Migration, Activation, and Effector Functions.

Front Cell Dev Biol. 2020-10-21

[4]
Actin reorganization at the centrosomal area and the immune synapse regulates polarized secretory traffic of multivesicular bodies in T lymphocytes.

J Extracell Vesicles. 2020-6-19

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PD-1 suppresses the maintenance of cell couples between cytotoxic T cells and target tumor cells within the tumor.

Sci Signal. 2020-9-15

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A dynamic CD2-rich compartment at the outer edge of the immunological synapse boosts and integrates signals.

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NCKAP1L defects lead to a novel syndrome combining immunodeficiency, lymphoproliferation, and hyperinflammation.

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HEM1 deficiency disrupts mTORC2 and F-actin control in inherited immunodysregulatory disease.

Science. 2020-7-10

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The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity.

Sci Immunol. 2020-7-10

[10]
LymphoAtlas: a dynamic and integrated phosphoproteomic resource of TCR signaling in primary T cells reveals ITSN2 as a regulator of effector functions.

Mol Syst Biol. 2020-7

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