Human Primary Immune Cells Exhibit Distinct Mechanical Properties that Are Modified by Inflammation |
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Authors: | Nathalie Bufi Michael Saitakis Stéphanie Dogniaux Oscar Buschinger Armelle Bohineust Alain Richert Mathieu Maurin Claire Hivroz Atef Asnacios |
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Affiliation: | 1.Laboratoire Matière et Systèmes Complexes, Université Paris-Diderot and CNRS, UMR 7057, Sorbonne Paris Cité, Paris, France;2.Institut Curie, Centre de Recherche, Pavillon Pasteur, Paris, France;3.Institut National de la Santé et de la Recherche Médicale, Unité 932, Immunité et Cancer, Paris, France |
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Abstract: | T lymphocytes are key modulators of the immune response. Their activation requires cell-cell interaction with different myeloid cell populations of the immune system called antigen-presenting cells (APCs). Although T lymphocytes have recently been shown to respond to mechanical cues, in particular to the stiffness of their environment, little is known about the rigidity of APCs. In this study, single-cell microplate assays were performed to measure the viscoelastic moduli of different human myeloid primary APCs, i.e., monocytes (Ms, storage modulus of 520 +90/−80 Pa), dendritic cells (DCs, 440 +110/−90 Pa), and macrophages (MPHs, 900 +110/−100 Pa). Inflammatory conditions modulated these properties, with storage moduli ranging from 190 Pa to 1450 Pa. The effect of inflammation on the mechanical properties was independent of the induction of expression of commonly used APC maturation markers, making myeloid APC rigidity an additional feature of inflammation. In addition, the rigidity of human T lymphocytes was lower than that of all myeloid cells tested and among the lowest reported (Young’s modulus of 85 ± 5 Pa). Finally, the viscoelastic properties of myeloid cells were dependent on both their filamentous actin content and myosin IIA activity, although the relative contribution of these parameters varied within cell types. These results indicate that T lymphocytes face different cell rigidities when interacting with myeloid APCs in vivo and that this mechanical landscape changes under inflammation. |
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