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Ann Clin Neurophysiol. 1999; 1(2): 91-98.
Histopathologic Features and CD5+ B-lymphocyte Expression in the Experimental Allergic Neuritis
Joong-Yang Cho, Won-Jun Choi, Sung-Hun Kim. Jung-J Sung, Ho-Jin Kim, Kyung-Seok Park, Ki-Young Choi, Hyun-Jung Kim, and Kwang-Woo Lee
Copyright © 1999 The Korean Society of Clinical Neurophysiology
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background : The pathogenesis of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), Guillain-Barr?syndrome (GBS) in not clear, but it has been known that the immune mechanisms play an important role. Authors performed this study to establish an animal model of experimental allergic neuritis(EAN) by immunizing the myelin components of peripheral nerves and to understand the electrophysiological and histopathological features as well as the CD5+ B-lymphocyte changes in peripheral bloods in the EAN models. Methods : Lewis rats weighing 150-200 gm were injected subcutaneously in soles two with total myelin, P0, P1, or P2 proteins purified from the bovine cauda eguina. The EAN induction was assessed by evaluating clinical manifestations. The electrophysiological and histopathological features were studied as routine methods. The CD5+ B-lymphocyte were double stained using monoclonal FITC conjugated anti-rat CD45RA and R-PE conjugated anti-rat CD5+antibodies and calculated using a fluorescence activated cell sorter (FACS). Results : The EAN animal models were established. In two out of five, in one out of two, in none out of three, and in none out of one Lewis rats injected with purified total myelin, P0, P1, P2 proteins respectively. They showed slow spontaneous motor activity and weak resistance against pulling back by tails. The typical electrophysiological and histologic findings in total protein and P0 induced EAN animal models were the decreased conduction velocity, the decreased compound muscle action potential (CMAP) amplitude and the dispersion phenomenon. The perivascular infiltrates of lymphocytes with focal demyelinating process were found in light microscopy. The CD5+ B-lymphocyte expression in three EANs were 2.38%, 3.50% 2.50%, which were not significantly increased, compared with those in normal controls. Conclusion : The EAN animal models were successfully established by injecting the total myelin and P0 myelin and they showed electrophysiological and histological features typical of demyelinating process. However they did not show an increased expression of CD5+ B-lymphocyte in peripheral bloods which could be indirect evidence of humoral autoimmunity.
Key words: Guillain Barre syndrome, Experimental allergic neuritis, Autoimmune disease
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