MARKED AMELIORATION OF ESTABLISHED COLLAGEN-INDUCED ARTHRITIS BY TREATMENT WITH ANTIBODIES TO CD23 IN-VIVO

CD23 is a low-affinity receptor for immunoglobulin E (IgE) expressed b y a variety of haematopoietic cells. Proteolytic cleavage of the trans nnembrane receptor generates soluble forms, which can be detected in b iological fluids. CD23 regulates many functional aspects of immune cel ls, both in its cell-associated and soluble forms. In view of the incr eased levels of CD23 in rheumatoid arthritis, we have studied the effe ct of neutralizing CD23 in type II collagen-induced arthritis in mice, a model for human rheumatoid arthritis. Successful disease modulation is achieved by treatment of arthritic DBA/1 mice with either polyclon al or monoclonal antibodies to mouse CD23. Treated mice show a dose-re lated amelioration of arthritis with significantly reduced clinical sc ores and number of affected paws. This improvement in clinical severit y is confirmed by histological examination of the arthritic paws. A ma rked decrease in cellular infiltration of the synovial sublining layer and limited destruction of cartilage and bone is evident in animals t reated with therapeutic doses of anti-CD23 antibody. These findings de monstrate the involvement of CD23 in a mouse model of human rheumatoid arthritis.