@article{93531,
  author = {Pacheco F and Prata R and Brandão SS and Ferreira H and Rodrigues T and Dos Santos JB and da Silva C and Tavares I and Mendes M and Rodrigues A and Machado A and Nery J and Amadeu TP and Moraes M and Sarno E and Schmitz V},
  title = {Erythema Nodosum Leprosum Neutrophil Subset Expressing IL-10R1 Transmigrates into Skin Lesions and Responds to IL-10.},
  abstract = {<p>Erythema nodosum leprosum (ENL) is an inflammatory complication in leprosy. Yet, the involvement of ENL neutrophils in the inflammatory response against  remains poorly explored. Our primary aim was to investigate the utility of the surface expression of neutrophil IL-10R1 as an ENL biomarker and, secondarily, to evaluate whether leprosy or healthy -stimulated neutrophils produce cytokines and are able to respond to IL-10. We, in this study, describe a subpopulation of circulating neutrophils of ENL patients that exclusively expressed IL-10R1, providing evidence that IL-10R1 neutrophils are present in ENL lesions. It was also found that ENL neutrophils, but not those of nonreactional leprosy controls, were able to secret detectable levels of TNF ex vivo and the addition of IL-10 blocked TNF release. It was likewise observed that stimulated, healthy neutrophils expressed IL-10R1 in vitro, and ENL-linked cytokines were released by -cultured neutrophils in vitro. Moreover, consistent with the presence of a fully functional IL-10R, the addition of IL-10 prevented the release of -induced cytokines. Most importantly, dead  revealed its superior capacity to induce  and  in primary neutrophils over live , suggesting that  may hamper the inflammatory machinery as an immune escape mechanism.</p>},
  year = {2020},
  journal = {ImmunoHorizons},
  volume = {4},
  pages = {47-56},
  month = {02/2020},
  issn = {2573-7732},
  url = {https://www.immunohorizons.org/content/4/2/47},
  doi = {10.4049/immunohorizons.1900088},
  language = {eng},
}