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B cell depletion is an effective remission induction and maintenance therapy in patients with antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV).1–6 Rituximab targets both pathogenic effector B cells and protective regulatory B cells. To avoid infections and adverse events from therapy, clinicians require improved markers of disease activity and impending relapse to guide immunosuppression strategies following B cell depletion. We reported that CD5+ B cells, as a surrogate marker of B regulatory cells, are decreased in patients with active AAV and normalise during disease remission.7 After B cell depletion, patients who repopulated with a low or decreasing percentage of CD5+ B cells and were on low maintenance immunosuppression had a shorter time to relapse than patients on similar levels of immunosuppression with normalised CD5+ B cells or patients with similarly low CD5+ B cells but higher immunosuppression. The CD5+CD24hiCD38hi B cell subpopulation correlates inversely with active disease but parallels both interleukin (IL)-10 production and suppression of ANCA.8 CD5 may identify B cells enriched in IL-10 production, the defining cytokine of B regulatory cells.8 ,9 Whether CD5+ B cells can serve as an indicator of time to relapse without considering remission maintenance immunosuppression dose is not known. We sought to address this question and confirm our previous findings in a larger cohort by separating patients solely based on their CD5+ B cells at repopulation.
We examined B cell phenotype in 50 patients with AAV following rituximab therapy by flow cytometry (table …