Serologic changes following B lymphocyte depletion therapy for XXXX .

@entity1 @entity32 @entity2225 @entity309 @entity1851
OBJECTIVE: To explore the changes in serologic variables and clinical disease activity following B lymphocyte depletion in 22 @entity1 with @entity309 ( @entity309 ). METHODS: B lymphocyte depletion was attained using combination therapy based on the monoclonal anti- @entity2225 antibody rituximab. Levels of a serologic indicator of @entity32 , @entity1851 ( @entity1851 ), of antimicrobial antibodies, of autoantibodies including IgA-, IgM-, and IgG-class rheumatoid factors (RF), and of antibodies to cyclic citrullinated peptide (anti-CCP) were assayed. RESULTS: The majority of @entity1 showed a marked clinical improvement after treatment with rituximab, with benefit lasting up to 33 months. Levels of total serum immunoglobulins fell, although the mean values each remained within the normal range. Whereas the IgM-RF response paralleled the changes in total serum IgM levels, the levels of IgA-RF, IgG-RF, and IgG and anti-CCP antibodies decreased significantly more than did those of their corresponding total serum immunoglobulin classes. The kinetics for the reduction in @entity1851 levels also paralleled the decreases in autoantibody levels. In contrast, levels of antimicrobial antibodies did not change significantly. B lymphocyte return occurred up to 21 months posttreatment. The time to relapse after B lymphocyte return was often long and unpredictable (range 0-17 months). Relapse was, however, closely correlated with rises in the level of at least one autoantibody. Increased autoantibody levels were rarely observed in the absence of clinical change. CONCLUSION: Following B lymphocyte depletion in @entity1 with @entity309 , a positive clinical response occurred in correlation with a significant drop in the levels of @entity1851 and autoantibodies. Antibacterial antibody levels were relatively well maintained. B lymphocyte return preceded relapse in all @entity1 . There was also a temporal relationship between clinical relapse and rises in autoantibody levels. Although these observations are consistent with a role for B lymphocytes in the pathogenesis of @entity309 , the precise mechanisms involved remain unclear.
