108 CHAPTER 5 cell clones during disease relapse. Such a study could prove that rituximab does not eradicate pathological B cells but just prevents them to reach the site of disease activity, i.e., the synovium, therefore explaining why - despite the temporary amelioration of disease symptoms - CD20-depleting therapy does not cure RA. Conclusions Using AIRR-sequencing to monitor the dynamics of B cell depletion and repopulation after rituximab treatment we observed that timing of depletion and repopulation does not predict response after 6 or 12 months. However, repopulation within 6 months did significantly correlate with response in the subsequent interval (6-12 months), suggesting it is repopulation rather than depletion that influences longterm remission. Based on our results, we hypothesize that interindividual differences in clinical response to rituximab are defined by patient-specific differences in B-cell turnover. We propose further studies are indicated to validate the latter observations, analyze the underlying mechanisms and assess which cell populations are involved.
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