Details

Autor(en) / Beteiligte

• Jamilloux, Yvan
• Henry, Thomas
• Belot, Alexandre
• Viel, Sébastien
• Fauter, Maxime
• El Jammal, Thomas
• Walzer, Thierry
• François, Bruno
• Sève, Pascal

Titel

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

Ist Teil von

• Autoimmunity reviews, 2020-07, Vol.19 (7), p.102567-102567, Article 102567

Ort / Verlag

Elsevier B.V

Erscheinungsjahr

2020

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• The 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. •COVID-19 induces both impairment and hyperactivation of the immune system.•Early viral clearance by type-I IFN is a key to preventing further viral replication, T cell exhaustion, and cytokine storm.•Timely administration of treatments may reduce viral load and avoid hyperinflammation.