Journal Article

DZNE-2026-01100

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png B Cells are Activated via a Nanoporous Interface that Stabilizes Microvilli and Engages Mechanosensitive Ion Channels.

Aghaizu, N. D. ; Weber, W. ; Strempel, N.DZNE* ; Polat, A. ; Klotzsch, E.

2026
Wiley-VCH Weinheim

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Please use a persistent id in citations: doi:10.1002/advs.76869

Abstract: B cell activation typically involves binding of presented antigen by the B cell receptor. Ensuing intracellular signaling with Ca2+ mobilization, cytoskeletal remodeling, and transcriptional changes culminates in an appropriate B cell response. Recently, our group developed an antigen receptor-independent, purely mechanobiological activation platform for T cells. Nanotopological stimulation by exposure to a porous membrane, resulted in robust T cell activation. Whether and how B cells are activated by this substrate on a mechanistic level is presently unknown. Here we report that nanoporous stimulation indeed results in B cell activation, where B cells extended nanopore penetrating microvilli and exhibited activation hallmarks including intracellular Ca2+ spikes, phosphorylation of signaling components, and cell surface expression of the activation marker cluster of differentiation (CD) 69, thus recapitulating T cell behavior. This is at least partially mediated by mechanosensitive cation channels, as determined by pharmacology. In summary, our findings demonstrate that B cells are amenable to antigen receptor-independent activation via nanopores, expanding our knowledge on B cell activation mechanisms.

Keyword(s): B-Lymphocytes: metabolism (MeSH) ; B-Lymphocytes: immunology (MeSH) ; Animals (MeSH) ; Nanopores (MeSH) ; Lymphocyte Activation: immunology (MeSH) ; Lymphocyte Activation: physiology (MeSH) ; Ion Channels: metabolism (MeSH) ; Mice (MeSH) ; Mechanotransduction, Cellular (MeSH) ; T-Lymphocytes: immunology (MeSH) ; T-Lymphocytes: metabolism (MeSH) ; B cell ; biology ; cell biology ; intracellular ; ion channel ; mechanosensitive channels ; nanomaterials ; pharmacology ; Ion Channels

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Contributing Institute(s):

1. Network Dysfunction (AG Schmitz)

Research Program(s):

1. 351 - Brain Function (POF4-351) (POF4-351)

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