TY - JOUR
T1 - Expression of CD23 in the germinal center of thymus from myasthenia gravis patients
AU - Murai, Hiroyuki
AU - Hara, Hideo
AU - Hatae, Tomoko
AU - Kobayashi, Takuro
AU - Watanabe, Takeshi
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 1997/6
Y1 - 1997/6
N2 - In order to investigate a pathogenic role of germinal centers which appear in the hyperplastic thymus of myasthenia gravis (MG) patients, we performed an immunohistochemical study using various monoclonal antibodies including CD23. In contrast with tonsilar germinal centers from non-MG individuals. CD23 was strongly and diffusely expressed in the whole area of germinal centers of MG thymi, including the outer zone. In addition, we measured the serum level of soluble CD23 (sCD23) in MG patients at various clinical stages. The high serum sCD23 levels, which were noted in the unthymectomized patients, fell to within normal range over 5 years after thymectomy, and the decline of serum sCD23 correlated well with clinical improvement. CD23 is thought to be responsible for preventing unselected germinal center B cells from entering apoptosis and, in turn, leads to the survival of auto-reactive B cell clones.
AB - In order to investigate a pathogenic role of germinal centers which appear in the hyperplastic thymus of myasthenia gravis (MG) patients, we performed an immunohistochemical study using various monoclonal antibodies including CD23. In contrast with tonsilar germinal centers from non-MG individuals. CD23 was strongly and diffusely expressed in the whole area of germinal centers of MG thymi, including the outer zone. In addition, we measured the serum level of soluble CD23 (sCD23) in MG patients at various clinical stages. The high serum sCD23 levels, which were noted in the unthymectomized patients, fell to within normal range over 5 years after thymectomy, and the decline of serum sCD23 correlated well with clinical improvement. CD23 is thought to be responsible for preventing unselected germinal center B cells from entering apoptosis and, in turn, leads to the survival of auto-reactive B cell clones.
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U2 - 10.1016/S0165-5728(97)00030-1
DO - 10.1016/S0165-5728(97)00030-1
M3 - Article
C2 - 9184633
AN - SCOPUS:0030904235
SN - 0165-5728
VL - 76
SP - 61
EP - 69
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -