TY - JOUR
T1 - Establishment of monoclonal antibodies against the extracellular domain that block binding of NMO-IgG to AQP4
AU - Miyazaki, Kaori
AU - Abe, Yoichiro
AU - Iwanari, Hiroko
AU - Suzuki, Yota
AU - Kikuchi, Takahiro
AU - Ito, Takashi
AU - Kato, Jungo
AU - Kusano-Arai, Osamu
AU - Takahashi, Toshiyuki
AU - Nishiyama, Shuhei
AU - Ikeshima-Kataoka, Hiroko
AU - Tsuji, Shoji
AU - Arimitsu, Takeshi
AU - Kato, Yasuhiro
AU - Sakihama, Toshiko
AU - Toyama, Yoshiaki
AU - Fujihara, Kazuo
AU - Hamakubo, Takao
AU - Yasui, Masato
N1 - Funding Information:
This work was supported by Global Center of Excellence Program for Humanoid Metabolomic Systems Biology of the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan ; Grant-in-Aid for Scientific Research B (General) of MEXT of Japan ( 21390061 ); the Japan New Energy and Industrial Technology Development Organization (NEDO , P08005 ); Keio University Special Grant-in-Aid for Innovative Collaborative Research Projects ; the NFAT project of the New Energy and Industrial Technology Development Organization (NEDO , P06009 ), Japan; Keio Gijuku Academic Development Funds ; and Japan Society for the Promotion of Science Grant-in-Aid for Scientific Research (C) ( 22590940 ).
PY - 2013
Y1 - 2013
N2 - Neuromyelitis optica is a demyelinating disease characterized by a disease-specific autoantibody designated as NMO-IgG that specifically recognizes aquaporin-4, and the binding of NMO-IgG to AQP4 causes the progress of the disease. Prevention of the binding of NMO-IgG, therefore, may alleviate the disease. Here we have developed monoclonal antibodies against AQP4 with a baculovirus display system in order to obtain high affinity monoclonal antibodies against the extracellular domains of AQP4. Our monoclonal antibodies can block the binding of NMO-IgG in spite of their heterogeneity. Taken together, we propose that our monoclonal antibodies can be applied in clinical therapy for NMO patients.
AB - Neuromyelitis optica is a demyelinating disease characterized by a disease-specific autoantibody designated as NMO-IgG that specifically recognizes aquaporin-4, and the binding of NMO-IgG to AQP4 causes the progress of the disease. Prevention of the binding of NMO-IgG, therefore, may alleviate the disease. Here we have developed monoclonal antibodies against AQP4 with a baculovirus display system in order to obtain high affinity monoclonal antibodies against the extracellular domains of AQP4. Our monoclonal antibodies can block the binding of NMO-IgG in spite of their heterogeneity. Taken together, we propose that our monoclonal antibodies can be applied in clinical therapy for NMO patients.
KW - Aquaporin-4
KW - Monoclonal antibody
KW - NMO-IgG
KW - Nueromyelitis optica
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U2 - 10.1016/j.jneuroim.2013.03.003
DO - 10.1016/j.jneuroim.2013.03.003
M3 - Article
C2 - 23746426
AN - SCOPUS:84878644469
SN - 0165-5728
VL - 260
SP - 107
EP - 116
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -