Antiidiotypic antibodies in renal transplantation
Blood transfusion given before transplantation may improve subsequent allograft survival but the mechanism of action remains unknown. Several groups have postulated that the blood transfusion effect in renal transplantation is mediated through idiotypic- antiidiotypic antibody interactions which result in specific immunosuppression. These antibodies were found to be directed towards both class I & II MHC antigens. Cyclosporin has been shown to be effective in abrogating a primary immune response (if administered concomitantly with blood transfusions) but not an established response. Recent studies have shown that antiidiotypic activity may be enhanced by cyclosporin, but the mechanism remains unknown. The main aims of the studies presented in this thesis were to investigate the idiotypic-antiidiotypic antibodies interaction in renal transplantation. Potentiating activity ('anti-antiidiotypic antibodies:Ab3') was also detected in non-cytotoxic sera from patients who were previously sensitised. Ab3 activity was induced following DST, but all patients who had this activity underwent successful transplantation. Cytotoxic sera were also found to contain Ab3 activity after absorption with platelets. The presence of Ab3 activity prior to transplantation or its subsequent development had no effect on graft survival or rejection episodes. These studies suggest that one mechanism by which blood transfusions improve graft survival is the development of antiidiotypic antibodies. Cyclosporin may enhance Ab2 activity if given during blood transfusion programmes.