The prolonged inability to up-regulate CD27 may inhibit the renewal of memory B cells. At the long term follow up, a reduction of CD27 + B cells was observed in blood and BM. ConclusionsĪnti-CD20 treatment achieves a depletion of IgD + B cells shortly after the treatment. The levels of rheumatoid factor decline after rituximab treatment but returned to baseline levels at the time of retreatment. A significant reduction of CD27 + cells in BM and in circulation was observed long after rituximab treatment (mean 22 months), while levels of naive B cells in BM and in circulation were increased. Analysis of the remaining BM B cells showed prevalence of immature and/or transitional B cells (CD38 ++CD24 ++) and CD27 +IgD - memory cells, while IgD + cells were completely depleted. One and three months following rituximab BM retained up to 30% of B cells while circulation was totally depleted of B cells. B cell populations were characterized by CD27/IgD/CD38/CD24 expression. Ten of these patients were resampled 1 month following rituximab, 14 patients after 3 months and the remaining 13 patients were included in the long-term follow up. Methodsīlood and BM samples were obtained from 37 patients with RA prior to rituximab treatment. In the present study we evaluated changes in the B cell phenotype in peripheral blood and bone marrow (BM) of patients with rheumatoid arthritis (RA) following anti-CD20 treatment using rituximab.
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