Pustular psoriasis is an inflammatory skin disease with features of neutrophil-mediated sterile autoinflammation. In this issue of JEM, Baldo et al. (https://doi.org/10.1084/jem.20231464) show that this autoinflammation is driven by a vicious cycle through neutrophil-derived IL-26.
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| http://dx.doi.org/10.1084/jem.20240229 | DOI Listing |
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Neutrophil IL-26 fuels autoinflammation.
J Exp Med
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Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary.
Pustular psoriasis is an inflammatory skin disease with features of neutrophil-mediated sterile autoinflammation. In this issue of JEM, Baldo et al. (https://doi.
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View Article and Find Full Text PDFHuman neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.
J Exp Med
May 2024
Department of Dermatology and Venereology, University Hospital of Lausanne, Lausanne, Switzerland.
Article Synopsis
- Autoinflammation involves a non-infectious inflammatory response where neutrophils and IL-1 cytokines play a key role, though the triggers are not well understood.
- In pustular psoriasis, neutrophils release a cytokine called IL-26, which promotes further autoinflammatory responses and attracts more neutrophils.
- The study highlights the role of IL-26 in linking neutrophils to a self-sustaining inflammatory loop, indicating its significance in the pathology of pustular psoriasis.
TLR4-mediated release of heparin-binding protein in human airways: a co-stimulatory role for IL-26.
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Background: Bacterial infection causes accumulation of neutrophils that release antimicrobial proteins including heparin-binding protein (HBP). In human airways, this neutrophil accumulation can be re-capitulated via intrabronchial exposure to lipopolysaccharide (LPS), a Toll-like receptor 4 (TLR4) agonist, that also causes a local increase in the neutrophil-mobilizing cytokine IL-26. Although LPS is considered a weak stimulus for HBP release , its effect on HBP release in human airways has not been characterized.
View Article and Find Full Text PDFAnti-glomerular Basement Membrane Disease Concomitant with MPO-ANCA Positivity Concurrent with High Serum Levels of Interleukin-26 Following Coronavirus Disease 2019 Vaccination.
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Division of Nephrology, Department of Internal Medicine, Teikyo University Chiba Medical Center, Japan.
As coronavirus disease 2019 (COVID-19) vaccine booster campaigns progress worldwide, new reports of complications following COVID-19 vaccination have emerged. We herein report a case of new-onset anti-glomerular basement membrane (GBM) disease concomitant with myeloperoxidase-antineutrophil cytoplasmic antibody positivity concurrent with high levels of interleukin (IL)-26 following the second dose of the Pfizer-BioNTech COVID-19 vaccine. The temporal association with vaccination in this case suggests that an enhanced neutrophilic immune response through IL-26 may have triggered necrotizing glomerulonephritis and a T-cell-mediated immune response to GBMs, leading to the development of anti-GBM antibodies, with an enhanced B-cell response after the vaccination triggering anti-GBM IgG and the onset of anti-GBM disease.
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