The role of gingival lymphocytes on the establishment of IgG dominant B cell lesion in periodontitis.

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Human periodontitis has been confirmed to be IgG producing cell rich lesion. We detected <T4^+> and <T8^+> cells as well as immunoglobulins, particularly IgG, producing cells in periodontal lesions. The incidence of HLA-DR(Ia) was also approximately equal in both <T4^+> and <T8^+> cell population. These results suggested that helper and suppressor functions could participate in the establishment of periodontal lesions.On the other hand, B cells might be activated polyclonally in periodontal lesion, because a variety of periodontal flora possessed polyclonal B cell activating capacities. We demonstrated that IgG antibody forming cells differentiated from surface IgG positive B cells but not from surface IgG negative B cells. The results suggested that the memory B cells primed with antigens might migrate into periodontal lesions, then they might be activated polyclonally and developed into IgG producing cells.Periodontal lesion could be, therefore, induced by the collaboration of the immunoregulatory mechanisms by T cells and macrophages with PBA. In fact, T cells, particularly helper/inducer T (Th/i) cells, enhanced IgG synthesis of B cells activated with T-independent B cell activators (TI-PBAs) such as LPS and Actinomyces viscosus preparation. Th/i cells were activated by recognition of Ia expressed on B cells. Ia increased on B cells stimulated with TI-PBAs. Activated Th/i cells produced soluble factors which enhanced IgG synthesis of B cells activated with TI-PBAs. T cells were strongly suggested to participate in the development of periodontal lesions.