Journal
NATURE COMMUNICATIONS
Volume 13, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-022-28172-4
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Funding
- MS Research Australia [16-122]
- Our Health in Our Hands a strategic initiative of the Australian National University
- Australian Government Research Training Program (RTP) Scholarship
- ACT Health Private Practice Trust Fund Grant
- Australian National Health and Medical Research Council [APP1052616]
- Sirtex Medical Ltd.
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This study reveals the mechanism by which neutrophil extracellular traps (NETs) directly activate T cells and specifically enhance Th17 cell differentiation. This suggests a direct link between neutrophils, NETs, and T cell autoimmunity.
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. Neutrophils are critical in the immune response to infective agents and have multiple effector strategies including the production of extracellular traps termed NETs. Here the authors show a link between NET production and Th17 differentiation which mechanistically occurs downstream of TLR2 signalling.
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