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免疫突触中RBL - 2H3肥大细胞受体动力学

RBL-2H3 Mast Cell Receptor Dynamics in the Immunological Synapse.

作者信息

Tsai Ming Chih, Spendier Kathrin

机构信息

Department of Physics and Energy Science, University of Colorado Colorado Springs, Colorado Springs, CO 80918, USA.

BioFrontiers Center, University of Colorado Colorado Springs, Colorado Springs, CO 80918, USA.

出版信息

Biophysica. 2022 Dec;2(4):428-439. doi: 10.3390/biophysica2040038. Epub 2022 Nov 7.

DOI:10.3390/biophysica2040038
PMID:37654558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10470655/
Abstract

The RBL-2H3 mast cell immunological synapse dynamics is often simulated with reaction-diffusion and Fokker-Planck equations. The equations focus on how the cell synapse captures receptors following an immune response, where the receptor capture at the immunological site appears to be a delayed process. This article investigates the physical nature and mathematics behind such time-dependent delays. Using signal processing methods, convolution and cross-correlation-type delay capture simulations give a -squared range of 22 to 60, in good agreement with experimental results. The cell polarization event is offered as a possible explanation for these capture delays, where polarizing rates measure how fast the cell polarization event occurs. In the case of RBL-2H3 mast cells, polarization appears to be associated with cytoskeletal rearrangement; thus, both cytoskeletal and diffusional components are considered. From these simulations, a maximum polarizing rate ranging from 0.0057 s to 0.031 s is obtained. These results indicate that RBL-2H3 mast cells possess both temporal and spatial memory, and cell polarization is possibly linked to a Turing-type pattern formation.

摘要

RBL - 2H3肥大细胞免疫突触动力学通常用反应扩散方程和福克 - 普朗克方程来模拟。这些方程关注的是细胞突触在免疫反应后如何捕获受体,其中免疫部位的受体捕获似乎是一个延迟过程。本文研究了这种时间依赖性延迟背后的物理本质和数学原理。使用信号处理方法,卷积和互相关类型的延迟捕获模拟给出的(R^2)范围为22至60,与实验结果高度吻合。细胞极化事件被认为是这些捕获延迟的一种可能解释,其中极化速率衡量细胞极化事件发生的速度。对于RBL - 2H3肥大细胞,极化似乎与细胞骨架重排有关;因此,细胞骨架和扩散成分都被考虑在内。从这些模拟中,获得了范围从0.0057 s至0.031 s的最大极化速率。这些结果表明RBL - 2H3肥大细胞具有时间和空间记忆,并且细胞极化可能与图灵型模式形成有关。

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1
RBL-2H3 Mast Cell Receptor Dynamics in the Immunological Synapse.免疫突触中RBL - 2H3肥大细胞受体动力学
Biophysica. 2022 Dec;2(4):428-439. doi: 10.3390/biophysica2040038. Epub 2022 Nov 7.
2
Antigen-dependent transition of IgE to a detergent-insoluble form is associated with reduced IgE receptor-dependent secretion from RBL-2H3 mast cells.IgE向去污剂不溶性形式的抗原依赖性转变与RBL-2H3肥大细胞中IgE受体依赖性分泌减少有关。
J Cell Physiol. 1990 Jul;144(1):128-36. doi: 10.1002/jcp.1041440117.
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RBL-2H3 cells are an imprecise model for mast cell mediator release.RBL-2H3细胞是肥大细胞介质释放的不精确模型。
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N-terminal amphipathic helix of Amphiphysin can change the spatial distribution of immunoglobulin E receptors (FcεRI) in the RBL-2H3 mast cell synapse.发动蛋白的N端两亲性螺旋可改变RBL-2H3肥大细胞突触中免疫球蛋白E受体(FcεRI)的空间分布。
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Substitution of an aspartic acid results in constitutive activation of c-kit receptor tyrosine kinase in a rat tumor mast cell line RBL-2H3.天冬氨酸的替换导致大鼠肿瘤肥大细胞系RBL - 2H3中c - kit受体酪氨酸激酶的组成型激活。
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Fc epsilon RI-mediated association of 6-micron beads with RBL-2H3 mast cells results in exclusion of signaling proteins from the forming phagosome and abrogation of normal downstream signaling.FcεRI介导的6微米珠子与RBL-2H3肥大细胞的结合导致信号蛋白被排除在形成的吞噬体之外,并消除正常的下游信号传导。
J Cell Biol. 1996 Sep;134(6):1427-39. doi: 10.1083/jcb.134.6.1427.

本文引用的文献

1
A theory of coalescence of signaling receptor clusters in immune cells.免疫细胞中信号受体簇的聚结理论。
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Self-organization principles of intracellular pattern formation.细胞内模式形成的自组织原理。
Philos Trans R Soc Lond B Biol Sci. 2018 May 26;373(1747). doi: 10.1098/rstb.2017.0107.
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Particle-based simulations of polarity establishment reveal stochastic promotion of Turing pattern formation.基于粒子的极性建立模拟揭示了图灵模式形成的随机促进。
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Cytoskeleton in mast cell signaling.细胞骨架在肥大细胞信号转导中的作用。
Front Immunol. 2012 May 25;3:130. doi: 10.3389/fimmu.2012.00130. eCollection 2012.
10
Single-particle tracking of immunoglobulin E receptors (FcεRI) in micron-sized clusters and receptor patches.免疫球蛋白 E 受体 (FcεRI) 在微米大小的簇和受体斑中的单颗粒跟踪。
FEBS Lett. 2012 Feb 17;586(4):416-21. doi: 10.1016/j.febslet.2012.01.013. Epub 2012 Jan 18.