| First Author | Wilson AS | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 528 |
| PubMed ID | 35082281 | Mgi Jnum | J:337167 |
| Mgi Id | MGI:6870172 | Doi | 10.1038/s41467-022-28172-4 |
| Citation | Wilson AS, et al. (2022) Neutrophil extracellular traps and their histones promote Th17 cell differentiation directly via TLR2. Nat Commun 13(1):528 |
| abstractText | 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. |
