The etiological significance of superantigen in periodontal disease and its possible role

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We demonstrated previously that superantigen (SAg) enhances CD80 expression on human monocytes, whereas treatment with SAg in the presence of lipopolysaccharide (LPS) markedly decreases the percentage of CD80ィイD1+ィエD1 peripheral blood monocytes, indicating that the presence of low levels of CD80 on monocytes inhibits CD27 expression on SAg-activated T cells due to insufficient delivery of positive signals via CD28/CD80 interaction. To assess the role of LPS in this inhibition, the relationship between SAg-dependent apoptosis and regulation of CD80 expression of CD14ィイD1+ィエD1 monocytes was examines. SAg enhanced the annexin V-positive or PI-positive (propidium iodide) levels in monocytes, whereas LPS-treated monocytes were resistant to the apoptotic action of SAg. This SAg-induced killing was abrogated by antagonists anti-CD95 (Fas) and anti-CD95 ligand monoclonal antibodies, suggesting a CD95-based pathway of apoptosis. Furthermore, apoptosis of monocytes, preferentially CD80ィイD1-ィエD1 monocytes, was affected by high-level expression of CD95 by SAg, and the survival required down-regulation of CD95 expression by LPS over the SAg action. During these culture periods, the number of CD80ィイD1+ィエD1 monocytes was nearly constant. These observations strongly suggested that a small fraction of CD80ィイD1+ィエD1 monocytes is selectively resistant to CD95-based apoptosis, and the percentage of CD80ィイD1+ィエD1 monocytes increases through escape from SAg-induced preferential apoptosis, which is inhibited by addition of LPS.