The detection of CD4+CD28- T-cells in other inflammatory conditions, such as psoriatic arthritis, MS, inflammatory bowel diseases (IBDs), cardiovascular diseases, chronic rejection, ankylosing spondylitis, and Wegener’s granulomatosis, has led to the hypothesis that HCMV-mediate induction of CD4+CD28− T-cells may be a shared mechanism of ADs [92,93,183,184]. This evidence concerns the gene CD28 and granulomatosis with polyangiitis.