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M9470109.TXT
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1994-07-02
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Document 0109
DOCN M9470109
TI Immunomodulation during treatment of polymyositis with plasmapheresis
and immunosuppressive drugs.
DT 9409
AU Dau PC; Department of Medicine, Evanston Hospital, IL 60201.
SO J Clin Apheresis. 1994;9(1):21-5. Unique Identifier : AIDSLINE
MED/94253025
AB Immunologic studies were carried out in a patient with polymyositis
(PM), who showed increasing muscle strength and decreasing serum
creatine phosphokinase levels during 20 weeks of treatment with
plasmapheresis in conjunction with prednisone and cyclophosphamide.
After an initial rise, serum IgG declined with treatment. Natural killer
(NK) lymphocytes were reduced by 74%, B cells by 95%, and T cells by
38%. Spontaneous proliferation of peripheral blood mononuclear cells
increased dramatically. Within the CD4+ T cell subset there was
increasing maturation as shown by a rise in percent mature (CD29+) cells
and reciprocal decline of immature (CD45RA+) cells. At the same time
CD4+ T cells became increasingly activated as shown by HLA-DR
expression. The percentage of CD8+ T cells increased strongly with
treatment, and they showed increased activation and expression of the
cytotoxic CD29+ and CD11b- phenotypes. CD8+ T cells exhibiting CD45RA or
CD11b+ suppressor phenotypes were overall unchanged; however, on
follow-up a proportion of CD8+ cells expressed the activated suppressor
effector (CD11b-CD28-) phenotype. In addition to control of PM by the
possible deletion of activated autoreactive B and T lymphocyte clones
with cyclophosphamide, the activation and maturation of CD4+ T cells
during treatment may have downregulated the autoreactive disease
process, either through direct antiidiotypic suppression or by induction
of the observed increase in cytotoxic and suppressor CD8+ T cells.
DE Adult Antigens, CD45/ANALYSIS Case Report CD4-CD8 Ratio Female
Human Immunosuppressive Agents/*THERAPEUTIC USE Phosphocreatine/BLOOD
*Plasmapheresis Polymyositis/IMMUNOLOGY/*THERAPY Support, Non-U.S.
Gov't T-Lymphocyte Subsets/IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).