OBJECTIVE: To investigate whether anti-CD4 antibodies can suppress experimental antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) induced by an anti-DNA monoclonal antibody (MAb). METHODS: BALB/c mice were treated with anti-CD4 MAb either before or 2 months after induction of experimental APS and SLE. Control mice were treated with rat IgG or phosphate buffered saline. Serologic and clinical manifestations of the disease were determined. RESULTS: Treatment of mice with anti-CD4 before or 2 months after disease induction prevented the development of experimental APS and SLE. The treated mice did not develop leukopenia or proteinuria, and had fewer episodes of fetal resorption. Similarly, the treated mice did not develop elevated erythrocyte sedimentation rate, prolonged activated partial thromboplastin time, or thrombocytopenia, and had significantly lower levels of antibodies to double-stranded DNA, histones, MIV-7, cardiolipin, and phosphatidylserine. Levels of CD4+ cells in the lymph nodes declined temporarily after the treatment and then returned to normal. CONCLUSION: Anti-CD4 antibodies can prevent experimental APS and SLE. These results may suggest a role for anti-CD4 treatment in human autoimmune diseases.
OBJECTIVE: To investigate whether anti-CD4 antibodies can suppress experimental antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) induced by an anti-DNA monoclonal antibody (MAb). METHODS: BALB/c mice were treated with anti-CD4 MAb either before or 2 months after induction of experimental APS and SLE. Control mice were treated with rat IgG or phosphate buffered saline. Serologic and clinical manifestations of the disease were determined. RESULTS: Treatment of mice with anti-CD4 before or 2 months after disease induction prevented the development of experimental APS and SLE. The treated mice did not develop leukopenia or proteinuria, and had fewer episodes of fetal resorption. Similarly, the treated mice did not develop elevated erythrocyte sedimentation rate, prolonged activated partial thromboplastin time, or thrombocytopenia, and had significantly lower levels of antibodies to double-stranded DNA, histones, MIV-7, cardiolipin, and phosphatidylserine. Levels of CD4+ cells in the lymph nodes declined temporarily after the treatment and then returned to normal. CONCLUSION: Anti-CD4 antibodies can prevent experimental APS and SLE. These results may suggest a role for anti-CD4 treatment in humanautoimmune diseases.