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自己免疫性神経疾患の発症機序:病原体・ガングリオシドとの分子相同性

自身免疫性神经系统疾病的发病机制：病原体和神经节苷脂的分子同源性

基本信息

批准号：
10780482
负责人：
結城伸泰
金额：
$ 0.83万
依托单位：
Dokkyo Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Encouragement of Young Scientists (A)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

軸索型ギラン・バレー症侯群モデル動物の樹立ウシ脳ガングリオシド注射後軸索型GBSのモデル動物の樹立を試みた.(1)ウサギ13羽に実際に使用されていたウシ脳ガングリオシド2.5mgもしくはFreund完全アジュバントを3週に1回の割合で感作を繰り返した.初回感作後5-11週で13羽全例に運動麻痺が生じた.発症からピークに達するまでの期間は4日から13日であり,GBS同様急性発症の様式をとった.末梢神経の大径有髄線維は著しく脱落し,ワーラー様の変性を呈していた.リンパ球の浸潤や脱髄像は見られなかった.これに対して,アジュバント対照群10羽では発症しなかった.(2)ウシ脳ガングリオシド感作ウサギでは,初回感作後2週ないし3週でIgMクラスの抗GM1抗体が誘導され,3週ないし4週でIgGへクラススイッチした.クラススイッチ後3週程度でIgG抗GM1抗体はピークに達し,その後1週以内に運動麻痺が発症する傾向がみられた.(3)ウサギ末梢神経よりガングリオシド画分を精製した.簿層クロマトグラム免疫染色にて,発症ウサギの血漿IgGが認識するバンドはモノシアロガングリオシド画分に存在し,標準GM1と同様の移動度を示した.さらに,発症ウサギの血漿IgGが認識するバンドを薄層クロマトグラム-blotting後に質量分析を行い,GM1に由来するシグナルが検出された.発症ウサギの血漿IgGが認識する分子がウサギ末梢神経に発現するGM1であることを確認した.正常ウサギの坐骨神経の軸索にコレラ毒素が結合し,GM1が末梢神経の軸索に発現していることを支持した.本研究により軸索型GBSの動物モデルが樹立されたことから,その病態の解明と治療法の開発は飛躍的に進むであろう.

The animals of the syndrome group were tested after injection. (1) after injection, the animals of the syndrome group were tested. (1) after injection, the animals of the syndrome group were tested. (1) after injection, the animals of the syndrome group were tested. (1) after injection, the animals of the syndrome group were tested. (1) after injection, the animals were tested. (1) after injection, the animals were tested. (1) after injection, the animal was tested. (1) after injection, the animal test was carried out. (1) after injection, the animal test was carried out. (1) after injection, the animal test was carried out. (1) after injection, the animal test was carried out. (1) after injection, the animal test was performed. (1) after injection, the animal was tested. (1) after injection, the animal was tested. (1) after injection, the animal was tested. (1) After the first feeling, 13 dogs were born after 5-11 exercise. The symptoms are similar to those with acute symptoms. GBS is the same as the acute syndrome. At the end of the road, there is a peel-off in the path, and the sex is in the shape of a knot. The ball is soaked and the ball falls off like a ball. In the group of 10 fetus, the disease was caused by the disease. (2) after the first sensation, the anti-GM1 antibody was detected in the first group of 10 fetus. (2) after the first feeling, the anti-GM1 antibody was detected in the first group of 10 fetus. (2) after the first feeling, the anti-GM1 antibody was detected in the first time, and the anti-GM1 antibody was detected in the first time. The level of IgG anti-GM1 antibody was detected at 3 degrees after treatment, and the symptoms of leprosy were detected within 1 year after treatment. (3) the terminal god was divided into two parts. The standard GM1 has the same degree of mobility as indicated by the presence of the standard GM1. After blotting, there was a quantitative analysis of the cause of the disease, and the cause of the disease was the cause of IgG. Symptoms, symptoms, IgG, knowledge, diagnosis, recognition, recognition, identification, recognition, identification, identification and confirmation. The normal sciatic nerve, the ischium, the epigastrium, the toxin, the toxin, the GM1, the tail, the end, the end, the end In this study, the animal model of GBS was used to determine the state of the disease and to understand the progress of clinical treatment.