SARS-CoV-2 infection stimulates a complex activation of the immune system . Eosinophils belong to the host's defense equipment against respiratory viruses . In the first phase of the infection, eosinophils contribution is probably appropriate and beneficial, as they facilitate the suppression of the viral replication . However, in severe COVID-19 patients, during the second and third phases of the disease, eosinophils may participate in a maladaptive immune response and directly contribute to immunopathology . In fact, in severe patients, the immune response is prevalently T helper 1 type, but T helper 2 is also present . Eosinophils' expansion and activation are stimulated by Type 2 cytokines, especially IL-5 . Moreover, bronchial asthma, in which eosinophils play a central role, seems not to be a major risk factor for severe COVID-19 . Among possible explanations, asthmatic patients are often treated with corticosteroids, which have been demonstrated to reduce the progression to critical COVID-19 in hospitalized patients . In addition to steroids, severe asthmatic patients are currently treated with biological drugs that target Type 2 immune response . Because IL-5 is necessary for the growth, survival, and activation of eosinophils, IL-5 inhibitors, such as mepolizumab, decrease the peripheral blood count of eosinophils, but do not influence eosinophils activation in the airway . In severe COVID-19 patients, the blockade of eosinophils' activation might contrast harmful immunity.
Index: COVID-19, anti-IL5 drugs, asthma, eosinophils, interleukin-5, type 2 response