Although B cell depletion therapy (BCDT) is now a well-accepted therapeutic option in autoimmune rheumatic disease, a significant proportion of patients remain resistant to therapy. .19pt?>A more challenging clinical problem is the high rate of relapse after B cell reconstitution, as well as the difficulty in predicting the exact timing of that relapse. In this article, we consider the immunological mechanisms that may account for the heterogeneity of clinical response to BCDT. Understanding how BCDT alters the balance between different B cell subsets, some pathogenic and some regulatory, may help us correctly target BCDT to the right patients, and thereby improve treatment responses in rheumatic disease.
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