Administration of adenovirus encoding anti-CD20 antibody gene induces B-cell deletion and alleviates lupus in the BWF1 mouse model

被引:1
作者
Wang, Chao [1 ]
Wang, Mian [2 ]
Liu, Yuan [1 ]
Zeng, Ping [1 ]
机构
[1] Gen Hosp Chengdu Army, Ctr Lab Dept, Chengdu 610083, Peoples R China
[2] Second Peoples Hosp Chengdu, Cardiovasc Dept, Chengdu 610017, Peoples R China
关键词
Adenovirus; Anti-CD20; antibody; B cells; Lupus; NON-HODGKINS-LYMPHOMA; IN-VITRO; RHEUMATOID-ARTHRITIS; HUMAN-DISEASE; MRL/LPR MICE; ERYTHEMATOSUS; RITUXIMAB; THERAPY; SLE; EXPRESSION;
D O I
10.1016/j.intimp.2011.01.014
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Increasing evidence demonstrates that pathological B cells play an essential role in the triggering and development of human systemic lupus erythematosus (SLE). A rational strategy for treating SLE might be to delete B cells thereby suppressing autoimmunity. Commercial monoclonal anti-CD20 antibody is widely used for treatment of B cell-related autoimmune disorders. However its long term use is limited by several factors including short half-life, high cost, and possible side effects of antibody protein therapy. Therefore, we constructed a recombinant adenovirus encoding the murine anti-CD20 antibody gene, and used it to immunize lupus-prone (BWF1) mice. Our data demonstrated that administration of adenovirus encoding the murine anti-CD20 antibody gene generated murine anti-CD20 antibody, which resulted in elimination of B cells in BWF1 mice. In addition, the anti-CD20 reduced serum anti-dsDNA antibody levels, impeded the development of proteinuria and improved the survival of BWF1 mice. These findings suggested that the adenovirus encoding murine anti-CD20 antibody gene might provide an alternative strategy for B cell-mediated diseases. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:693 / 697
页数:5
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