B10 cells characterized as CD5+CD1dhighB cells have been shown to produce abundant IL-10 and ameliorate EAE and DSS-induced colitis,[12,28] while CD5+CD24highCD38high B cells have been reported to attenuate anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis by IL-10-production.[29] However, despite multiple mechanistic studies of the CD5-signaling pathway in B cells,[30] it remains unclear whether CD5 is induced by activation or arises from separate precursors through distinctive development. This evidence concerns the gene IL10 and vasculitis.