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TLR7 activation in M-CSF-dependent monocyte-derived human macrophages potentiates inflammatory responses and prompts neutrophil recruitment

التفاصيل البيبلوغرافية
العنوان: TLR7 activation in M-CSF-dependent monocyte-derived human macrophages potentiates inflammatory responses and prompts neutrophil recruitment
المؤلفون: Simón-Fuentes, Miriam, Herrero, Cristina, Acero-Riaguas, Lucía, Nieto, Concha, Lasala, Fátima, Labiod, Nuria, Luczkowiak, Joanna, Alonso, Bárbara, Delgado, Rafael, Colmenares, María, Corbí, Angel L., Domínguez-Soto, Ángeles
المساهمون: Ministerio de Ciencia e Innovación (España), Fundación BBVA, Fundació La Marató de TV3, Instituto de Salud Carlos III, European Commission, Fundación "la Caixa", Red de Investigación en Enfermedades Reumáticas (España), Consejo Superior de Investigaciones Científicas (España), Simón-Fuentes, Miriam, Acero-Riaguas, Lucía, Nieto, Concha, Lasala, Fátima, Labiod, Nuria, Luczkowiak, Joanna, Alonso, Bárbara, Delgado, Rafael, Colmenares, María b, Corbí, Angel L., Domínguez-Soto, Ángeles
بيانات النشر: Karger Publishers
سنة النشر: 2023
المجموعة: Digital.CSIC (Consejo Superior de Investigaciones Científicas / Spanish National Research Council)
الوصف: 23 p.-5 fig. ; 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. ; This work was supported by Grant PID2020-114323RB-I00 from Ministerio de Ciencia e Innovación, “Ayudas FUNDACIÓN BBVA a equipos de investigación científica SARS-CoV-2 y COVID-19” and Grant 201619.31 from Fundació La Marató/TV3 to ALC, grants from the Instituto de Investigación Carlos III, ISCIII,(PI2100989), European Commission Horizon 2020 FP (Project VIRUSCAN FETPROACT-2016: ID 731868), Horizon Europe FP (Project EPIC-CROWN-2 ID: 101046084) and Fundación Caixa-Health Research (Project StopEbola HR18-00469) to RD, and Red de Investigación en Enfermedades Reumáticas (RIER, RD16/0012/0007), and ...
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1662-811X
1662-8128
العلاقة: #PLACEHOLDER_PARENT_METADATA_VALUE#; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2020-114323RB-I00/ES/POLARIZACION Y RE-PROGRAMACION DE MACROFAGOS HUMANOS POR SEROTONINA: PAPEL DEL ARYL HYDROCARBON RECEPTOR (AHR) Y LOS FACTORES LXR Y SREBP/; info:eu-repo/grantAgreement/EC/H2020/731868; Postprint; https://doi.org/10.1159/000530249Test; Sí; Journal of Innate Immunity (2023); http://hdl.handle.net/10261/306731Test
DOI: 10.1159/000530249
الإتاحة: https://doi.org/10.1159/000530249Test
http://hdl.handle.net/10261/306731Test
حقوق: open
رقم الانضمام: edsbas.29E2E47C
قاعدة البيانات: BASE
الوصف
تدمد:1662811X
16628128
DOI:10.1159/000530249