       Document 0070
 DOCN  M9630070
 TI    High levels of TH2 cytokine gene expression in systemic lupus
       erythematosus.
 DT    9603
 AU    Richaud-Patin Y; Alcocer-Varela J; Llorente L; Departamento de
       Inmunologia y Reumatologia, Instituto Nacional; de la Nutricion Salvador
       Zubiran, Mexico, D.F.
 SO    Rev Invest Clin. 1995 Jul-Aug;47(4):267-72. Unique Identifier : AIDSLINE
       MED/96030315
 AB    Systemic lupus erythematosus (SLE) is an autoimmune disease with a clear
       imbalance in the network made up of different cytokines. However this
       statement has been derived from studies which have focused on the
       analysis of some specific cytokines and few have simultaneously analyzed
       those cytokines that could be involved in the pathogenesis of SLE.
       Therefore, we decided to analyze interleukin IL-1b, IL-2, IL-4, IL-6,
       IL-10, tumor necrosis factor-a (TNF-a) and gamma interferon (IFN-g) gene
       expression in peripheral blood mononuclear cells from 17 women with SLE
       and 10 normal females by a coupled reverse transcriptase-polymerase
       chain reaction technique. High gene expression of IL-4, IL-6, IL-10 and
       TNF-a was found in SLE patients as compared to normal subjects. The
       expression of IL-1b, IL-2 and IFN-g genes was low or undetectable. The
       resulting high level of cytokines with strong effect on proliferation
       and differentiation of B lymphocytes in SLE could be responsible for the
       characteristic B cell hyperactivity and autoantibody production seen in
       SLE.
 DE    Adolescence  Adult  B-Lymphocytes/METABOLISM  Base Sequence  Female
       *Gene Expression Regulation  Human  Interferon Type
       II/*BIOSYNTHESIS/GENETICS  Interleukins/*BIOSYNTHESIS/GENETICS  Lupus
       Erythematosus, Systemic/BLOOD/*GENETICS  Middle Age  Molecular Sequence
       Data  Polymerase Chain Reaction  RNA, Messenger/ANALYSIS  Support,
       Non-U.S. Gov't  Th2 Cells/*METABOLISM  Tumor Necrosis
       Factor/*BIOSYNTHESIS/GENETICS  JOURNAL ARTICLE

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

