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Título: | TLR7 activation in M-CSF-dependent monocyte-derived human macrophages potentiates inflammatory responses and prompts neutrophil recruitment |
Autor: | Simón-Fuentes, Miriam CSIC ORCID ; Herrero, Cristina CSIC; Acero-Riaguas, Lucía; Nieto, Concha; Lasala, Fátima; Labiod, Nuria; Luczkowiak, Joanna; Alonso, Bárbara CSIC; Delgado, Rafael; Colmenares, María ; Corbí, Angel L. ; Domínguez-Soto, Ángeles CSIC | Fecha de publicación: | 11-abr-2023 | Editor: | S. Karger AG | Citación: | Journal of Innate Immunity (2023) | Resumen: | Toll-like receptor 7 (TLR7) is an endosomal Pathogen-Associated Molecular Pattern (PAMP) receptor that senses single-stranded RNA (ssRNA) and whose engagement results in the production of type I IFN and pro-inflammatory cytokines upon viral exposure. Recent genetic studies have established that a dysfunctional TLR7-initiated signaling is directly linked to the development of inflammatory responses. We present evidences that TLR7 is preferentially expressed by monocyte-derived macrophages generated in the presence of M-CSF (M-MØ). We now show that TLR7 activation in M-MØ triggers a weak MAPK, NFκB and STAT1 activation and results in low production of type I IFN. Of note, TLR7 engagement re-programs MAFB+ M-MØ towards a pro-inflammatory transcriptional profile characterized by the expression of neutrophil-attracting chemokines (CXCL1-3, CXCL5, CXCL8), whose expression is dependent on the transcription factors MAFB and AhR. Moreover, TLR7-activated M-MØ display enhanced pro-inflammatory responses and a stronger production of neutrophil-attracting chemokines upon secondary stimulation. As aberrant TLR7 signaling and enhanced pulmonary neutrophil/lymphocyte ratio associate with impaired resolution of virus-induced inflammatory responses, these results suggest that targeting macrophage TLR7 might be a therapeutic strategy for viral infections where monocyte-derived macrophages exhibit a pathogenic role. | Descripción: | 23 p.-5 fig. | Versión del editor: | https://doi.org/10.1159/000530249 | URI: | http://hdl.handle.net/10261/306731 | DOI: | 10.1159/000530249 | ISSN: | 1662-811X | E-ISSN: | 1662-8128 |
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