Human T cell-dependent B cell differentiation induced by staphylococcal superantigens.

摘要: Microbial superantigens (SAgs), by virtue of their binding to TCR V beta elements on T cells and class II MHC molecules accessory (AC), trigger cell activation. Although anti-CD3 mAb (which also activation via surface CD3/TCR) can readily induce cell-dependent B differentiation in unmanipulated PBMC cultures, induction Ig production SAg-stimulated cultures has usually required special manipulation the cells, such as irradiating them or treating with mitomycin C. We now demonstrate that eight different staphylococcal SAgs, typically at concentrations 10- 100-fold lower than those for proliferation, each peripheral blood tonsil drive polyclonal differentiation. Such SAg-induced generation Ig-secreting (IgSC) requires only occurs absence monocytes long there are adequate numbers serve (DR+) AC. Physical contact among responder AC (when from cells) is required. The fusion protein CTLA4Ig inhibits IgSC a dose-dependent fashion, whereas control no effect. In contrast, has, best, modest effects indicating CD28 (CTLA4)/B7 (B7-like) interactions play more prominent role proliferation. These results establish useful model cell/B interactions, inasmuch other types necessary successful differentiation; these importance (B7-like)-dependent mechanisms this process.