Abstract
Forty-two percent of the sera from patients undergoing chronic hemodialysis contained cold-reactive IgM antibodies reactive to autologous lymphocytes when tested by both complement-dependent microcytotoxicity assay and indirect immunofluorescence. In contrast, none of the 114 sera tested had IgG autolymphocytotoxins. The latter finding pertained even for those sera that contained IgG alloantibodies reactive to 99% of the random donor panel. IgG autolymphocytotoxins were, however, transiently present (few months) in those patients that had recently rejected a living related kidney allograft. The broadly reactive IgM alloantibody could be removed from the serum by absorption with autologous cells, thus indicating that the antigenic determinants were commonly shared by both autologous and allogeneic cells. The broadly reactive IgG alloantibody could be absorbed out by cells from a single allogeneic donor, but not autologous donor, indicating that the IgG-reactive alloantigen is a commonly shared alloantigen but apparently absent on autologous cells. The mechanism by which autoalloantigen (on lymphocytes) escape detection from the very broadly reactive IgG alloantibody (>99% PRA) but not the IgM antibody is difficult to understand. The role of alloantigen immunization in causing autoantibody formation was also investigated. No corelation existed between the presence or development of IgM autoantibodies with blood transfusions or kidney allografts. Yet, such alloantigen stimulation led to both IgG and IgM alloantibody formation. Finally, the role of autoantibody in modulating B lymphocyte function was analyzed by corelating the degree of alloantibody response to alloantigens with the presence or absence of autoantibody. A significant corelation existed between the presence of IgM autoantibody and the absolute quantity of IgG alloantibodies. However, the autoantibody did not prevent sensitization to alloantigens.