May contribute to acute inflammation through release of IFN-γ, GM-CSF, IL-10, IL-17A, IL-17F, IL-21, and IL-22 (155);Appear to be proportionally upregulated in COVID-19 (as compared to Treg (156), which may be associated with clinical outcome (156); may be a mechanism for COVID-19-related autoimmunity (155). This evidence concerns the gene IL17F and Autoimmunity.