Published: 22 October 2021
Author(s): Corrado Campochiaro, Alessandro Tomelleri, Marco Matucci-Cerinic, Lorenzo Dagna
Issue: January 2022
Section: Editorial

In severe coronavirus disease 2019 (COVID-19) patients, SARS-CoV-2 infection induces a systemic immune activation characterized by an afinalistic release of inflammatory cytokines [1,2]. This dysfunctional response often ends up into a multi-organ damage and can be responsible for a significant, and sometimes irreversible, clinical deterioration [3]. In this scenario, the pro-inflammatory cytokine interleukin (IL)-6 has been universally recognized as a key player [1]. Moreover, its central role in COVID-19 has been further corroborated by the clinical evidence that serum levels of IL-6, and of its surrogate C-reactive protein, correlate with disease severity and patients’ outcome [3].


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