CD28 and anti-neutrophil cytoplasmic antibody-associated vasculitis: This hypothesis has been recently substantiated by a proof of concept study showing that, in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), the expansion of CD28- T-cells was reduced by an antiviral therapy able to suppress HCMV subclinical reactivation, indicating that expansion of this clone was HCMV-dependent [96].