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MAFB and MAF Transcription Factors as Macrophage Checkpoints for COVID-19 Severity

AuthorsVega, Miguel A. CSIC ORCID ; Simón-Fuentes, Miriam CSIC ORCID ; González de la Aleja, Arturo ; Nieto, Concha CSIC ORCID ; Colmenares, María CSIC ORCID ; Herrero, Cristina; Domínguez-Soto, Ángeles CSIC ; Corbí, Angel L. CSIC ORCID
Innate immunity
Issue Date18-Nov-2020
PublisherFrontiers Media
CitationFrontiers in Immunology 11: 603507 (2020)
AbstractDefective IFN production and exacerbated inflammatory and pro-fibrotic responses are hallmarks of SARS-CoV-2 infection in severe COVID-19. Based on these hallmarks, and considering the pivotal role of macrophages in COVID-19 pathogenesis, we hypothesize that the transcription factors MAFB and MAF critically contribute to COVID-19 progression by shaping the response of macrophages to SARS-CoV-2. Our proposal stems from the recent identification of pathogenic lung macrophage subsets in severe COVID-19, and takes into consideration the previously reported ability of MAFB to dampen IFN type I production, as well as the critical role of MAFB and MAF in the acquisition and maintenance of the transcriptional signature of M-CSF–conditioned human macrophages. Solid evidences are presented that link overexpression of MAFB and silencing of MAF expression with clinical and biological features of severe COVID-19. As a whole, we propose that a high MAFB/MAF expression ratio in lung macrophages could serve as an accurate diagnostic tool for COVID-19 progression. Indeed, reversing the macrophage MAFB/MAF expression ratio might impair the exacerbated inflammatory and profibrotic responses, and restore the defective IFN type I production, thus becoming a potential strategy to limit severity of COVID-19.
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Appears in Collections:(VICYT) Colección Especial COVID-19
(CIB) Artículos

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