5. AIHAにおける溶血機序：マクロファージの役割

抄録

In vitro interaction between peripheral blood monocytes and the antibody-sensitized human erythrocytes was studied morphologically and with the ⁵¹Cr release assay. IgG antibody-sensitized human erythrocytes (EA) were phagocytized easily by monocytes in vitro when incubated at 37°C for 60 min, but it was inhibited competitively by the addition of free IgG in the medium. Complement-coated erythrocytes, without IgG sentization, were bound by monocytes as rosette fashion but not ingested even after incubation at 37°C for 60 min. Chromium release assay revealed that the sensitized erythrocytes were killed extracellularly by monocytes and it was enhanced by the addition of Cytochalasin B. Simultaneous sensitization of EA with complement component (C 3) also enhanced the lysis by monocytes and overcame the inhibitory effect of fluid phase IgG. Complement-coated erythrocytes per se were not lysed by monocytes in vitro but significant ⁵¹Cr release was observed after the addition of Cytochalasin B. These finding suggested that the lysis of erythrocytes by monocytes occurred extracellularly by the release of lysosomal enzymes. Non-sensitized chromium-labelled erythrocytes, when incubated with non-labelled EA and monocytes, were not lysed by monocytes even though Cytochalasin B was added. It was suggested that the lytic action of lysosomal enzymes was effective to the erythrocytes directly attached to the monocyte surface through Fc or C 3 receptors but did not affect to the neighboring normal erythrocytes.
Cytolytic activity of monocytes from patients with inflammatory diseases was enhanced compared to that of normal persons. Monocytes from patients with AIHA also showed enhanced capacity to phagocytize the autologous sensitized erythrocytes. The sensitization (arming) of monocytes with antierythrocyte autoantibodies seemed to be a factor responssible for this monocyte activation in AIHA.