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1994-07-02
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Document 0066
DOCN M9470066
TI [Pathogenesis of Graves' disease]
DT 9409
AU Yokoyama N; Nagataki S; First Department of Internal Medicine, Nagasaki
University School; of Medicine.
SO Nippon Rinsho. 1994 Apr;52(4):1110-7. Unique Identifier : AIDSLINE
MED/94254232
AB The discovery of long acting thyroid stimulator in Graves' disease and
autoantibodies specific for the thyroid in Hashimoto disease in 1956,
were the earliest examples of autoimmune responses. Autoimmune thyroid
disease has many important advantages in the investigation of autoimmune
disease when compared to the other disease. It is possible to obtain
thyroid tissue at biopsy and to investigate the histology by various
methods and the interactions between thyrocytes and infiltrated
mononuclear cells in vitro. Important autoantigens, such as the TSH
receptor, thyroid peroxidase and thyroglobulin have already been cloned
and each autoantigen has a specific function. Furthermore, we can
observe precisely the clinical course of the disease using laboratory
parameters. In this review, the pathogenesis of Graves' disease will be
overviewed using the results obtained, mainly in our laboratory, in the
following topics: (1) Immunogenetics: HLA class I and II, Gm, multiple
genes (2) Trigger: bacteria, retrovirus (HIV, HTLV-I), radiation (3)
Initiation and perpetuation of autoimmune responses: role of HLA class I
and II antigens, characteristics of infiltrated mononuclear cells,
interactions among thyrocytes, mononuclear cells and endothelial cells,
role of cytokines, adhesion molecules (4) Autoantibodies: methods of
determination and clinical correlates of TSH receptor antibodies (5)
Autoantigens: structure and functional relationship of TSH receptor (6)
Future studies: possible methods of treatment based on pathogenesis, a
model of new treatment.
DE Autoantibodies Cell Adhesion Molecules Cytokines English Abstract
Graves' Disease/*ETIOLOGY/GENETICS/IMMUNOLOGY Human HIV HLA Antigens
IgG Radiation Injuries JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).