Deficiency of neutrophil membrane antigen detected by monoclonal antibody in rheumatoid arthritis

Abstract
Monoclonal antibodies (mAbs) against cell surface antigens and receptors are instrumental in defining specific membrane markers. mAbs GF26.7.3 and MF25.1 against human neutrophils modulated the activation mechanism of superoxide anion production induced by formyl‐peptide and PMA in all subjects. However, treatment with mAb MF 25.1 binds is absent in rheumatoid conditions. This confirms our previous data showing that defective expression of membrane components is associated with neutrophil dysfunction.