Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
Serologic changes following B lymphocyte depletion therapy for rheumatoid arthritis
  • Publication Type:
    Journal article
  • Publication Sub Type:
  • Authors:
    Cambridge G, Leandro MJ, Edwards JC, Ehrenstein MR, Salden M, Bodman-Smith M, Webster AD
  • Publication date:
  • Pagination:
    2146, 2154
  • Journal:
    Arthritis and Rheumatism
  • Volume:
  • Issue:
  • Print ISSN:
  • Keywords:
    ABSENCE, activity, administration & dosage, adult, Aged, 80 and over, AGENT, AGENTS, Anti-Inflammatory Agents, Antibacterial, antibodies, Antibodies, Monoclonal, Antibody, Antimicrobial, Antineoplastic Agents, Antirheumatic Agents, Arthritis, Rheumatoid, Autoantibodies, B-Lymphocytes, benefit, Blood, C REACTIVE PROTEIN, C-Reactive Protein, C-REACTIVE-PROTEIN, Class, clinical, COMBINATION, COMBINATION THERAPIES, COMBINATION THERAPY, Correlation, Cyclophosphamide, cytology, DEPLETION, disease, drop, drug therapy, factors, Female, Iga, IgG, Igm, IM, IMMUNOGLOBULIN, Immunoglobulin A, IMMUNOGLOBULIN G, Immunoglobulin M, IMMUNOGLOBULINS, immunology, IMPROVEMENT, INDICATOR, Inflammation, kinetic, Kinetics, LA, LEVEL, LONG, LYMPHOCYTE, Lymphocyte Depletion, Lymphocytes, M, Male, MECHANISM, mechanisms, metabolism, Methods, Middle Aged, Observation, PATHOGENESIS, Patient, patients, peptide, positive, Prednisolone, PROTEIN, RANGE, Recurrence, REDUCTION, RELAPSE, relationship, response, Result, Rheumatoid arthritis, Rheumatoid Factor, RHEUMATOID-ARTHRITIS, RISE, serum, Support, Non-U.S.Gov't, therapy, TIME, treatment, VALUES, variable, VARIABLES, Arthritis
OBJECTIVE: To explore the changes in serologic variables and clinical disease activity following B lymphocyte depletion in 22 patients with rheumatoid arthritis (RA). METHODS: B lymphocyte depletion was attained using combination therapy based on the monoclonal anti-CD20 antibody rituximab. Levels of a serologic indicator of inflammation, C-reactive protein (CRP), 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 patients 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 CRP 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 patients with RA, a positive clinical response occurred in correlation with a significant drop in the levels of CRP and autoantibodies. Antibacterial antibody levels were relatively well maintained. B lymphocyte return preceded relapse in all patients. 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 RA, the precise mechanisms involved remain unclear
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Div of Medicine
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by