Erythema Nodosum Leprosum Neutrophil Subset Expressing IL-10R1 Transmigrates into Skin Lesions and Responds to IL-10

• Published in: ImmunoHorizons 2020-02, Vol.4 (2), p.47-56
• Main Authors: Pacheco, Fabiana Santos, Prata, Rhana Berto da Silva, Brandão, Sheila Santos, Ferreira, Helen, Rodrigues, Thaís Fernanda, Brandão Dos Santos, Jéssica, da Silva, Camila Oliveira, Tavares, Isabella Forasteiro, Mendes, Mayara Abud, Rodrigues, Ana Carolina Duarte Pereira, Machado, Alice de Miranda, Nery, José Augusto da Costa, Amadeu, Thaís Porto, Moraes, Milton Ozório, Sarno, Euzenir Nunes, Schmitz, Veronica
• Format: Article
• Language: English
• ISSN: 2573-7732; 2573-7732
• DOI: 10.4049/immunohorizons.1900088

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.