Аннотация:%transitional cells (r2 ¼ 0.69, P < 0.0001) and plasmablasts (r2 ¼ 0.61, P < 0.0001) in RTX-N patients, but not in RTX-T patients.In RTX-N patients, BAFF levels and %BAFF-R þ B-cells were negatively correlated in total CD19 þ B-cells (r2 ¼ 0.49, P ¼ 0.0003), in naive B-cells (r2 ¼ 0.51, P ¼ 0.0002); and in post-switched B-cells (IgD-CD27þ) (r2 ¼ 0.5, P ¼ 0.0002).No such correlations were found after RTX.In RTX-N patients, there was a positive correlation between BAFF levels and total IgM and autoantibodies to dsDNA (r2 ¼ 0.53, 0.48, respectively; P < 0.005 for both) with median anti-dsDNA levels 908 IU (RTX-N) but not in RTX-T patients (median anti-dsDNA 558 IU).Conclusion: These results suggest that (IgDþ and IgD-) CD38þþ B-cells were differently sensitive to BAFF-mediated effects in RTX-N patients, compared with RTX-T patients.RTX treatment may therefore disrupt the aberrant interaction between BAFF and B-cells in RTX-N SLE patients.Serum anti-dsDNA antibodies and total IgM also correlated with BAFF levels in RTX-N patients but not in RTX-T.RTX treatment, may therefore remove pathogenic autoantibodies/immune complexes, which may be responsible for altering the functional consequences of both apparently disparate CD38þþ B cell subpopulations driven by BAFF.
