Immunologic rebound

Authors

  • Peter C. Dau M.D.

    Corresponding author
    1. Department of Medicine, Divisions of Allergy/Immunology and Neurology, Evanston Hospital, Evanston
    2. Department of Neurology, Northwestern University Medical School, Chicago, Illinois
    • Department of Medicine. Evanston Hospital, 2650 Ridge Avenue, Evanston, IL60201
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Abstract

Evidence for accelerated specific antibody (Ab) rebound or overshoot after single or multiple therapeutic plasmapheresis (TP) is fragmentary but suggested by both clinical and experimental evidence. In vitro studies showing increased peripheral blood lymphocyte turnover and total immunoglobulin production after a series of TP without immunosup-pression may signify a generalized immunostimulation through removal of regulatory molecules by TP. It is known that IgG class Ab can down regulate B cells by cross linkage of their Ag and Fc receptors. Cyclophosphamide and other cytotoxic immunosuppressive agents effectively delete proliferating lymphocytes. TP could particularly foster deletion of lymphocytes actively mediating autoimmunity, since they would be more readily stimulated to proliferation by removal of Ab or other inhibitory factors than the generally resting normal immune system. This is supported by a relatively greater reduction of autoantibody levels than total immunoglobulin after treatment with TP and cytotoxic immunosuppressives.

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