小兒科Tchorbanov, Andrey?I.Andrey?I.TchorbanovVoynova, Elisaveta?N.Elisaveta?N.VoynovaMihaylova, Nikolina?M.Nikolina?M.MihaylovaTodorov, Todor?A.Todor?A.TodorovNikolova, MariaMariaNikolovaYomtova, Vihra?M.Vihra?M.YomtovaChiang, Bor-LuenBor-LuenChiangVassilev, Tchavdar?L.Tchavdar?L.Vassilev2008-12-052018-07-112008-12-052018-07-112007http://ntur.lib.ntu.edu.tw//handle/246246/88659The pathological DNA-specific B lymphocytes in lupus are logical targets for a selected therapeutic intervention. We have hypothesized that it should be possible to suppress selectively the activity of these B cells in lupus mice by administering to them an artificial molecule that cross- links their surface immunoglobulins with the inhibitory Fc gamma IIb surface receptors. A hybrid molecule was constructed by coupling the DNA- mimicking DWEYSVWLSN peptide to a monoclonal anti-mouse Fc gamma RIIb antibody. This chimeric antibody was added to cultured spleen cells from sick MRL/1pr mice, immunized with diphtheria toxoid, resulting in reduction of the numbers of anti-DNA but not of anti-diphtheria IgG antibody-producing cells. Intravenous infusions with the DNA-peptide antibody chimera to 7-wk-old animals prevented the appearance of IgG anti- DNA antibodies and of albuminuria in the next 2 months. The administration of the DNA-peptide chimeric antibody to 18 wk-old mice with full-blown disease resulted in the maintenance of a flat level of IgG anti-DNA antibodies and in delay of the aggravation of the lupus glomerulonephritis . The use of chimeric antibodies targeting inhibitory B lymphocyte receptors represents a novel approach for the selective suppression of autoreactive disease-associated B cells in autoimmune diseases.en-USautoreactive B cellsFc gamma IIb receptorsystemic lupuserythematosusjournal article