       Document 0150
 DOCN  M9610150
 TI    Suppression of experimental autoimmune myasthenia gravis after CD8
       depletion is associated with decreased IFN-gamma and IL-4.
 DT    9601
 AU    Zhang GX; Ma CG; Xiao BG; Bakhiet M; Ljungdahl A; Olsson T; Link H;
       Division of Neurology, Karolinska Institute, Huddinge University;
       Hospital, Stockholm, Sweden.
 SO    Scand J Immunol. 1995 Oct;42(4):457-65. Unique Identifier : AIDSLINE
       MED/96017847
 AB    CD8+ T cells can perform both Th1- and Th2-like functions by producing
       cytokines such as interferon-gamma (IFN-gamma) and interleukin-4 (IL-4),
       as well as the immune response down-regulating transforming growth
       factor-beta (TGF-beta), which are all involved in the development of
       experimental autoimmune myasthenia gravis (EAMG), a model for human MG.
       We have reported that depletion of CD8+ T cells results in the
       suppression of EAMG accompanied by the down-regulation of AChR-specific
       B cell responses and AChR-reactive IFN-gamma secreting Th1-like cells.
       To identify the involvement of IFN-gamma, IL-4 and TGF-beta in the
       development of EAMG after CD8+ T cell depletion, the expression of mRNA
       for these cytokines was studied in mononuclear cells from popliteal,
       inguinal and mesenteric lymph nodes, spleen and thymus by adopting in
       situ hybridization with complementary DNA oligonucleotide probes.
       Depletion of CD8+ T cells resulted in decreased levels of IFN-gamma and
       IL-4 mRNA expressing cells in different lymphoid organs except thymus,
       but no change in the numbers of TGF-beta mRNA expressing cells. The
       results imply that the suppression of EAMG after depletion of CD8+ T
       cells is caused by decreasing the effector factors but not by increasing
       the suppressor factor(s).
 DE    Animal  Autoimmunity  Cell Count  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY/PATHOLOGY  Disease Models, Animal
       Down-Regulation (Physiology)  Female  Immunophenotyping  Interferon Type
       II/*BIOSYNTHESIS  Interleukin-4/*BIOSYNTHESIS  Lymphoid
       Tissue/IMMUNOLOGY/METABOLISM/PATHOLOGY  Myasthenia
       Gravis/*IMMUNOLOGY/PATHOLOGY  Rats  Rats, Inbred Lew  RNA,
       Messenger/ANALYSIS  Support, Non-U.S. Gov't  Transforming Growth Factor
       beta/BIOSYNTHESIS  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

