Should we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions

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Autor(es): dc.creatorJamilloux, Yvan-
Autor(es): dc.creatorHenry, Thomas-
Autor(es): dc.creatorBelot, Alexandre-
Autor(es): dc.creatorViel, Sébastien-
Autor(es): dc.creatorFauter, Maxime-
Autor(es): dc.creatorEl Jammal, Thomas-
Autor(es): dc.creatorWalzer, Thierry-
Autor(es): dc.creatorFrançois, Bruno-
Autor(es): dc.creatorSève, Pascal-
Data de aceite: dc.date.accessioned2026-02-09T11:39:11Z-
Data de disponibilização: dc.date.available2026-02-09T11:39:11Z-
Data de envio: dc.date.issued2020-05-25-
Data de envio: dc.date.issued2020-05-25-
Data de envio: dc.date.issued2020-05-
Fonte completa do material: dc.identifierhttps://repositorio.ufla.br/handle/1/41216-
Fonte completa do material: dc.identifierhttps://www.sciencedirect.com/science/article/pii/S1568997220301294-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1144424-
Descrição: dc.descriptionThe coronavirus disease-19 pandemic (COVID-19), which appeared in China in December 2019 and rapidly spread throughout the world, has forced clinicians and scientists to take up extraordinary challenges. This unprecedented situation led to the inception of numerous fundamental research protocols and many clinical trials. It quickly became apparent that although COVID-19, in the vast majority of cases, was a benign disease, it could also develop a severe form with sometimes fatal outcomes. Cytokines are central to the pathophysiology of COVID-19; while some of them are beneficial (type-I interferon, interleukin-7), others appear detrimental (interleukin-1β, -6, and TNF-α) particularly in the context of the so-called cytokine storm. Yet another characteristic of the disease has emerged: concomitant immunodeficiency, notably involving impaired type-I interferon response, and lymphopenia. This review provides an overview of current knowledge on COVID-19 immunopathology. We discuss the defective type-I IFN response, the theoretical role of IL-7 to restore lymphocyte repertoire, as well as we mention the two patterns observed in severe COVID-19 (i.e. interleukin-1β-driven macrophage activation syndrome vs. interleukin-6-driven immune dysregulation). Next, reviewing current evidence drawn from clinical trials, we examine a number of cytokine and anti-cytokine therapies, including interleukin-1, -6, and TNF inhibitors, as well as less targeted therapies, such as corticosteroids, chloroquine, or JAK inhibitors.-
Idioma: dc.languageen-
Publicador: dc.publisherElsevier-
Direitos: dc.rightsrestrictAccess-
???dc.source???: dc.sourceAutoimmunity Reviews-
Palavras-chave: dc.subjectSevere Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)-
Palavras-chave: dc.subjectCOVID-19-
Palavras-chave: dc.subjectCytokine storm-
Palavras-chave: dc.subjectTocilizumab-
Palavras-chave: dc.subjectAnakinra-
Palavras-chave: dc.subjectType-I interferon-
Título: dc.titleShould we stimulate or suppress immune responses in COVID-19? Cytokine and anti-cytokine interventions-
Tipo de arquivo: dc.typeArtigo-
Aparece nas coleções:Repositório Institucional da Universidade Federal de Lavras (RIUFLA)

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