Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2541734 | International Immunopharmacology | 2011 | 5 Pages |
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.
Research highlights► We constructed a recombinant adenovirus encoding the murine anti-CD20 antibody gene to immunize BWF1 mice. ► Administration of the adenovirus eliminated B cells and reduced serum anti-dsDNA antibody levels. ► Administration of the adenovirus impeded the development of proteinuria and improved the survival of BWF1 mice. ► The adenovirus might provide an alternative strategy for B cell-mediated diseases.