Nephrology Dialysis Transplantation, Vol 13, Issue 1 160-164, Copyright © 1998 by Oxford University Press
K Smith, N Isbel, M Catton, J Leydon, G Becker and R Walker
Background: No conventional immunosuppressive agent
preferentially inhibits antibody production. Studies in experimental
animals and in human cells in vitro suggested
mycophenolate mofetil (MMF) might have such an effect. If this was the case
in vivo it could have significant implications in
terms of both MMF toxicity and the rational design of immunotherapeutic
regimens. Methods: Subjects were renal transplant
recipients (25 patients treated with prednisolone, cyclosporine and
azathiprine, and 13 treated with prednisolone, cyclosporine and MME) and 20
normal controls. The three groups received influenza vaccination, and the
antibody response to it was measured 4-6 weeks later using a standard
haemagglutination assay. Results: MMF profoundly
suppressed the humoral immune response to influenza vaccination when added
to prednisolone and cyclosporine. This effect could be seen when comparing
the rise in the mean titre of antibody after vaccination. It was also
reflected in the number of patients mounting responses deemed to be
clinically protective by either demonstrating a 4-fold rise in titre or an
increase in titre to ⩾50. Conclusions:
Suppression of the humoral immune response by MMF has implications for the
design of immunization protocols to protect the immunosuppressed, and
raises the possibility that MMF use may be accompanied by more or different
infections than complicate more conventional immunosuppression. More
importantly, consideration should be given to harnessing the relatively
specific effect of MMF on antibody production to treat antibody-mediated
diseases. Key words: antibodies; humoral immunity;
influenza vaccination; mycophenolate mofetil; renal transplantation
ORIGINAL ARTICLES
Suppression of the humoral immune response by mycophenolate mofetil
Department of Nephrology, Royal Melbourne Hospital, Parkville, Victoria, Australia; Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, UK; Victorian Infectious Diseases Reference Laboratory, Fairfield, Victoria, Australia; Corresponding author at: Department of Medicine, University of Cambridge School of Clinical Medicine, Box 157, Addenbrooke's Hospital, Cambridge, CB2 2QQ, UK
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