Immune Adherence Reactions of Human Erythrocytes Sensitized with Complement In Vitro and In Vivo

Abstract Human erythrocytes and erythrocyte stroma sensitized in vitro with antibody and complement are reactive in immune adherence (I.A.). This was demonstrated by using isoantibodies (anti-A, anti-Lea) and with autoantibodies obtained from patients with the cold hemagglutinin syndrome or paroxysmal cold hemoglobinuria (P.C.H.). Although trypsin destroys the I.A. receptor site on human erythrocytes used as indicator particles, it did not diminish the ability of the cells to fix complement and participate in I.A. as the antigen-antibody-complement complex. Erythrocytes from patients with warm antibody autoimmune hemolytic anemia (A.I.H.A.), the cold hemagglutinin syndrome, or P.C.H., which were strongly sensitized in vivo with C3 as judged by agglutination tests (and stroma prepared from such erythrocytes), were uniformly negative in I.A., indicating a lack of biologic reactivity of cell-bound C3 in these disease states. Paroxysmal nocturnal hemoglobinuria (P.N.H.) erythrocytes lysed by fresh acidified normal human serum were negative in I.A., in striking contrast to positive results obtained with the same concentration of stroma of erythrocytes sensitized with complement by isoantibodies or autoantibodies. Erythrocytes that had fixed C3 by mechanisms possibly of a nonimmunologic nature were negative in I.A. Although quantitative factors may be the explanation for negative immune adherence in some of these test systems, qualitatively different C3 fixation may also account for such findings. The I.A. receptor site on human erythrocytes was shown to be present on P.N.H. erythrocytes and umbilical cord erythrocytes and was not inhibited by sensitization with a variety of isoantibodies or penicillin. However, the erythrocytes of one of 13 patients with warm antibody A.I.H.A. gave negative results when used as indicator particles, and the autoantibody in this patient's serum inhibited the I.A. receptor site of normal erythrocytes.