Abstract
It is presumed that the B cell rich lesion characteristic for periodontitis could be induced by oral microorganisms. One of the mechanisms would be Polyclonal B cell activation (PBA). Actinomyces viscosus was shown to be such an activator, but the mechanism in detail is not still well understood. In this report, the requirement of immunocompetent cells (T cells and macrophages) for PBA and the development of IgG producing plasma cells as well as IgM were investigated in the murine system by using water soluble sonicate extract from A. viscosus T 14V (A. v. sup), and discussed the mechanism of the establishment of the IgG secreting plasma cell rich lesion.
The following results were drawn:
1. A. v. sup activated B cells polyclonally without any T cells and macrophages. Splenic B cells from CBA/N mice (xid) strongly responded to A. v. sup. These above results demonstrated that A. v. sup had a PBA activity such as TI-1 antigens.
2. A. v. sup induced IgG antibody-forming cells (AFC) as well as IgM AFC polyclonally. IgG AFC was induced from surface IgG positive (sIgG+) B cells (so called memory B cells) which had been primed with an antigen, but not from sIgG- B cells.
Although these results did not manifest the direct evidence that B cell lesion in periodontitis could be induced by the PBA activity, they supported that the PBA activity could concern in the establishment of the IgG secreting plasma cell rich lesion in periodontitis.
