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1996-02-27
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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).