anti-idiotypic antibody specific to gad65 autoantibody prevents type 1 diabetes in the nod mouseanti-idiotypic抗体针对gad65自身抗体预防1型糖尿病nod小鼠.pdfVIP

anti-idiotypic antibody specific to gad65 autoantibody prevents type 1 diabetes in the nod mouseanti-idiotypic抗体针对gad65自身抗体预防1型糖尿病nod小鼠.pdf

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anti-idiotypic antibody specific to gad65 autoantibody prevents type 1 diabetes in the nod mouseanti-idiotypic抗体针对gad65自身抗体预防1型糖尿病nod小鼠

Anti-Idiotypic Antibody Specific to GAD65 Autoantibody Prevents Type 1 Diabetes in the NOD Mouse 1 . 2. 3 1 4 5 6 Xin Wang * , Aixia Zhang , Yu Liu , Shi Chen , Zhenqing Feng , Wenbin Shang , Marlena Maziarz , 6 6 Jared Radtke , Christiane S. Hampe * 1 Department of Endocrinology, Jiangsu Province Hospital of TCM, Nanjing, Jiangsu, China, 2 School of Pharmacy, Nanjing Medical University, Nanjing, Jiangsu, China, 3 Department of Endocrinology, 2nd Hospital of Jilin University, Changchun, Jilin, China, 4 Key Laboratory of Antibody Technology of Ministry of Health, Nanjing Medical University, Nanjing, Jiangsu, China, 5 Medical Research Center, First College of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China, 6 University of Washington, Seattle, Washington, United States of America Abstract Overt autoantibodies to the smaller isoform of glutamate decarboxylase (GAD65Ab) are a characteristic in patients with Type 1 diabetes (T1D). Anti-idiotypic antibodies (anti-Id) directed to GAD65Ab effectively prevent the binding of GAD65 to GAD65Ab in healthy individuals. Levels of GAD65Ab-specific anti-Id are significantly lower in patients with T1D, leading to overt GAD65Ab in these patients. To determine the possible protective role of GAD65Ab-specific anti-Id in T1D pathogenesis, we developed the monoclonal anti-Id MAb 8E6G4 specifically targeting human monoclonal GAD65Ab b96.11. MAb 8E6G4 was demonstrated as a specific anti-Id directed to the antigen binding site of b96.11. MAb 8E6G4 recognized human antibodies in sera from healthy individuals, T2D patients, and T1D patients as established by ELIS

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