New monoclonal anti-human Fc gamma receptor II antibodies induce platelet aggregation

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Abstract
We developed two new monoclonal antibodies, designaled NNKY3‐2 and NNKY4‐7, that recognized a 40‐kD platelet protein. They appeared to be monoclonal anti‐Fc gamma receptor II (FC‐/RII) antibodies from the results of flow cytometric binding inhibition studies using another monoclonal anti‐FcγRII antibody (2E1). The addition of NNKY3‐2 or NNKY4‐7 to platetet‐rich plasma (PRP) led to a typical aggregation pattern preceded by a lag phase, but their addition to washed platelets did not induce aggregation. The aggregation of PRP by these antibodies was inhibited by prostaglandin E1 (PGE1) or staurosporine (protein kinase C inhibitor), whereas it was only slightly affected by a monoclonal anti‐GPIIb/IIIa antibody or Arg‐Gly‐Asp‐Ser, Furthermore, these antibodies induced the aggregation of washed platelets plus normal serum, but not that of washed platelets plus heat‐treatcd serum (destruction of complement activity). These results suggest that NNKY3‐2 or NNKY4‐7‐induced aggregation involves an unusual pathway independent of fibrinogen, and that the important factor is the participation of complement. NNKY3‐2 and NNKY4‐7 may be useful to study the relationship between autoantibodies, the Fc receptor, and complement in idiopathic thrombocytopenic purpura.