T cell stiffness is enhanced upon formation of immunological synapse

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Abstract

T cells are activated by target cells via an intimate contact, termed immunological synapse (IS). Cellular mechanical properties, especially stiffness, are essential to regulate cell functions. However, T cell stiffness at a subcellular level at the IS still remains largely elusive. In this work, we established an atomic force microscopy (AFM)-based elasticity mapping method on whole T cells to obtain an overview of the stiffness with a resolution of ~ 60 nm. Using primary human CD4⁺ T cells, we show that when T cells form IS with stimulating antibody-coated surfaces, the lamellipodia are stiffer than the cell body. Upon IS formation, T cell stiffness is enhanced both at the lamellipodia and on the cell body. Chelation of intracellular Ca²⁺ abolishes IS-induced stiffening at the lamellipodia but has no influence on cell body-stiffening, suggesting different regulatory mechanisms of IS-induced stiffening at the lamellipodia and the cell body.

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All data generated or analysed during this study are included in the manuscript, figure supplements or source data files. All files are uploaded.

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Philipp Jung

Institute for Medical Microbiology and Hygiene, Saarland University, Homburg, Germany

Competing interests
The authors declare that no competing interests exist.
Xiangda Zhou

Biophysics, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, Homburg, Germany

Competing interests
The authors declare that no competing interests exist.
Sandra Iden

Saarland University, Homberg, Germany

Competing interests
The authors declare that no competing interests exist.
Markus Bischoff

Biophysics, Center for Integrative Physiology and Molecular Medicine (CIPMM), Saarland University, Homburg, Germany

Competing interests
The authors declare that no competing interests exist.
Bin Qu

Biophysics, Saarland University, Homburg, Germany

For correspondence
bin.qu@uks.eu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-9382-3203

Funding

Deutsche Forschungsgemeinschaft (SFB1027 A2)

Bin Qu

Deutsche Forschungsgemeinschaft (SFB1027 B2)

Markus Bischoff

Deutsche Forschungsgemeinschaft (SPP1782 ID79/2-2)

Sandra Iden

Leibniz-Gemeinschaft (INM Fellowship)

Bin Qu

Deutsche Forschungsgemeinschaft (SFB1027 A12)

Sandra Iden

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

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This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.