[S-17-1] 超微形態から見たCIDPの病態：ランビエ絞輪・傍絞輪部に対する自己抗体の意義

小池春樹 (名古屋大学病院脳神経内科)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-2] CIDPにおけるランビエ絞輪部・傍絞輪部に対する自己抗体

緒方英紀¹, 山﨑亮², 吉良潤一² (1.九州大学病院脳神経内科, 2.九州大学大学院医学研究院神経内科学)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-3] 抗自律神経節アセチルコリン受容体抗体と自己免疫性自律神経節障害

中根俊成^1,2, 安東由喜雄¹ (1.熊本大学病院脳神経内科, 2.熊本大学病院　分子神経治療学寄附講座)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.

[S-17-4] 抗plexin D1抗体と有痛性ニューロパチー

藤井敬之, 山﨑亮, 吉良潤一 (九州大学大学院医学研究院　神経内科学)

Newly discovered autoantibodies that react with the specific sites of peripheral nerves produces unique clinical manifestations and laboratory findings, such as neuropathic pain, autonomic symptoms, nerve hypertrophy, and axo-glial detachment. These manifestations might be originated from antibody-antigen interaction at specific sites such as nodes of Ranvier, paranodes, posterior ganglion small neurons, and autonomic ganglia. This symposium encompasses anti-neurofascin155 and -contactin1 antibodies targeting the paranodes, anti-plexinD1 antibody targeting the primary pain-conducting neurons, and anti-ganglionic acetylcholine receptor antibody targeting the autonomic ganglia. These autoantibodies could be not only diagnostic biomarkers but also pathogenic. The purpose of this symposium is to deepen the knowledge about the mechanism and cascade of events leading to the specific manifestations of neuropathy by each autoantibody.