Experimental autoimmune myasthenia gravis and CD5+ B-lymphocyte expression.
10.3346/jkms.1999.14.1.75
- Author:
Kwang Woo LEE
1
;
Sung Hyun LEE
;
Ho Jin KIM
;
Jong Min KIM
;
Yoo Mi CHOI
;
Massakatsu MOTOMURA
Author Information
1. Department of Neurology, College of Medicine, Seoul National University, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Myasthenia gravis;
Disease model, animal;
Autoimmune diseases;
Antigen, CD5;
Acetylcholine receptors
- MeSH:
Animal;
Antigens, CD5/immunology*;
B-Lymphocytes/immunology*;
Disease Models, Animal;
Myasthenia Gravis/immunology*;
Myasthenia Gravis/chemically induced;
Rats;
Rats, Inbred Lew
- From:Journal of Korean Medical Science
1999;14(1):75-79
- CountryRepublic of Korea
- Language:English
-
Abstract:
Myasthenia gravis is one of the typical organ specific autoimmune disease and the CD5+ B-lymphocytes are known to be associated with the secretion of autoimmune antibodies. The authors performed the study to establish an animal model of experimental autoimmune myasthenia gravis (EAMG) by immunizing the nicotinic acetylcholine receptor (AChR) and to understand CD5+ B-lymphocyte changes in peripheral blood of EAMGs. Lewis rats weighing 150-200 g were injected subcutaneously three times with 50 microg AChR purified from the electric organ of Torpedo marmorata and Freund's adjuvant. The EAMG induction was assessed by evaluating clinical manifestations. The CD5+ B-lymphocyte was double stained using monoclonal PE conjugated anti-CD5+ and FITC conjugated anti-rat CD45R antibodies and calculated using a fluorescence-activated cell sorter (FACS). In three out of ten Lewis rats injected with purified AChR, the EAMG models were established. The animals showed definite clinical weakness responded to neostigmine; they had difficulty in climbing the slope, or easily fell down from a vertical cage. The range of CD5+ B-lymphocytes of peripheral blood in the EAMG models was 10.2%-17.5%, which was higher than in controls. In conclusion, the EAMG models were successfully established and the CD5+ B-lymphocyte expression in peripheral blood increased in EAMGs. This provided indirect evidence of the autoimmune pathomechanism of human myasthenia gravis.
