Publication Date:
1999-11-27
Description:
The hallmark of rheumatoid arthritis (RA) is specific destruction of the synovial joints. In a mouse line that spontaneously develops a disorder with many of the features of human RA, disease is initiated by T cell recognition of a ubiquitously expressed self-antigen; once initiated, pathology is driven almost entirely by immunoglobulins. In this study, the target of both the initiating T cells and pathogenic immunoglobulins was identified as glucose-6-phosphate isomerase, a glycolytic enzyme. Thus, some forms of RA or related arthritides may develop by a mechanism fundamentally different from the currently popular paradigm of a joint-specific T cell response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsumoto, I -- Staub, A -- Benoist, C -- Mathis, D -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1732-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (CNRS/INSERM/ULP), BP 163, 67404 Illkirch, C.U. de Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576739" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antigen Presentation
;
Antigen-Antibody Complex/immunology/metabolism
;
Arthritis, Rheumatoid/*immunology
;
Autoantibodies/*immunology
;
Autoantigens/*immunology
;
B-Lymphocytes/*immunology
;
Cross Reactions
;
Disease Models, Animal
;
Glucose-6-Phosphate Isomerase/chemistry/*immunology
;
Humans
;
Immunoglobulins/immunology
;
Joints/immunology
;
Mice
;
Mice, Inbred C57BL
;
Mice, Inbred NOD
;
Mice, Transgenic
;
Recombinant Fusion Proteins/immunology
;
T-Lymphocytes/*immunology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
