Neutrophil extracellular traps and their histones promote Th17 cell differentiation directly via TLR2

Alicia S. Wilson, Katrina L. Randall, Jessica A. Pettitt, Julia I. Ellyard, Antje Blumenthal, Anselm Enders, Benjamin J. Quah, Tobias Bopp, Christopher R. Parish and Anne Brüstle ()
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Alicia S. Wilson: The Australian National University
Katrina L. Randall: The Australian National University
Jessica A. Pettitt: The Australian National University
Julia I. Ellyard: The Australian National University
Antje Blumenthal: The University of Queensland Diamantina Institute, The University of Queensland
Anselm Enders: The Australian National University
Benjamin J. Quah: The Australian National University
Tobias Bopp: Institute for Immunology, University Medical Center, Johannes Gutenberg University Mainz
Christopher R. Parish: The Australian National University
Anne Brüstle: The Australian National University

Nature Communications, 2022, vol. 13, issue 1, 1-12

Abstract: Abstract Neutrophils perform critical functions in the innate response to infection, including through the production of neutrophil extracellular traps (NETs) - web-like DNA structures which are extruded from neutrophils upon activation. Elevated levels of NETs have been linked to autoimmunity but this association is poorly understood. By contrast, IL-17 producing Th17 cells are a key player in various autoimmune diseases but are also crucial for immunity against fungal and bacterial infections. Here we show that NETs, through their protein component histones, directly activate T cells and specifically enhance Th17 cell differentiation. This modulatory role of neutrophils, NETs and their histones is mediated downstream of TLR2 in T cells, resulting in phosphorylation of STAT3. The innate stimulation of a specific adaptive immune cell subset provides an additional mechanism demonstrating a direct link between neutrophils, NETs and T cell autoimmunity.

Date: 2022
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DOI: 10.1038/s41467-022-28172-4

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