B cell activation induced by superantigens

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It is now widely accepted that superantigens (SAgs), by binding to TCR Vb elements on T cells and to MHC class II molecules on accessory cells, stimulate T cells expressing particular TCR Vb chains. As SAg-activated T cells, having wide variety of antigen specificities, are supposed to be polyclonal by nature, they may then induce the activation of polyclonal B cells including autoreactive B cells. This possibility is now providing a basis for the hypothesis that SAgs may play important roles in the induction of autoimmune diseases.Theoretically there are two possible mechanisms by which B cells might be polyclonally activated by SAgs ; first, SAgs stimulate B cells directly by acting as MHC class II ligands. Second, as mentioned above, SAgs stimulate B cells indirectly by virtue of their ability to mediate T/B interaction.We first examine the direct effect of SAgs on accessory cells. The experiments using mouse macrophage cell lines and human B cell lines showed that certain bacrerial SAgs stimulated directly macrophages and B cells to secrete cytokines but that all bacterial SAgs tested inhibited Ig secretion from B cells. Next, we examine the net-effects including the direct and indirect actions of SAgs on B Cell activation. The experiments using unseparated human PBMC showed that bacterial SAg stimulated B cells to secrete Ig transienty in the early phase (3 days post stimulation) but finally inhibited the secretion by 7 days post stimulation.In conclusion, although there still remains the possibility that superantigens may activate particular types of autoreactive B cells by specific activation of autoreactive T cells, it seems unlikely that autoreactive B cells can be activated by the mechanism of polyclonal B cell activation directly or indirectly induced by SAg stimulation.