The effects of exogenous interleukin-12 on the induction of immune response to Porphyromonas gingivalis in vivo in mice.

The effects of treatment with exogenous interleukin-12 (IL-12) on the induction of immune response to Porphyromonas gingivalis, a black pigmented periodontopathic oral bacterium in mice, were determined in the present study. An increased footpad swelling representing a delayed type hypersensitivity (DTH) response to P. gingivalis in IL-12-treated mice could be observed, although increasing doses of IL-12 did not produce cumulative effects on this cellular Immune response. Multiple injections with IL-12 also resulted in elevated serum IFN-gamma levels. Treatment with this cytokine the day before, on and after immunization with heat-killed P. gingivalis augmented the levels of serum antigen-specific IgG2a and IgG3 antibodies, but had obviously little or no effects on those of serum antigen-specific IgG1 and IgG2b antibodies. The results of this study suggest that treatment with exogenous IL-12 In P. gingivalis-immunized mice may enhance DTH response and Th1 cell-associated antibody production.

Nitric oxide production by murine spleen cells stimulated with Porphyromonas gingivalis-derived lipopolysaccharide.

The aim of the present study was to determine whether Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) may stimulate nitric oxide (NO) production by murine spleen cells. Spleen cells derived from Balb/c mice were cultured in the presence of Pg-LPS or LPS from Salmonella Typhosa. The cell were also cultured in the presence of Pg-LPS with or without L-arginine, L-arginine plus NG-monomethyl-L-arginine (NMMA), or IFN-gamma. Furthermore, the plastic non-adherent spleen cells were stimulated with Pg-LPS and L-arginine. The results showed that Pg-LPS failed to stimulate splenic NO production by themselves. Exogenous L-arginine or IFN-gamma up-regulated the NO production of Pg-LPS-stimulated spleen cells, but the stimulatory effects of L-arginine were completely blocked by NMMA. It was also demonstrated that in the presence of Pg-LPS and L-arginine, splenic macrophages were the cellular source of NO. These results suggest, therefore, that P. gingivalis-LPS may induce murine splenic macrophages to produce NO in a L-arginine and an IFN-gamma-dependent mechanism.

The role of T lymphocytes in Sjögren's syndrome.

The exact role of T cells in the immunopathogenesis of Sjögren's syndrome (SS) is not well understood and is discussed herein. It seems plausible that this autoimmune disorder is associated strongly with the functions of autoantigen-specific CD4 cells. T cell receptor Vbeta gene usage appears to be unrestricted. Furthermore, elevated gene expression of T cell-derived cytokines such as IFN-gamma, IL-1, IL-6, IL-10 and IL-13 seen in salivary glands of SS patients and the animal models of this disorder suggests that the course of SS may be mediated by Th1 and Th2 cells. Defining the precise role of these CD4 cells subsets in SS would certainly provide insights into the establishment of immunotherapeutic bimodal.

The immunology of nickel-induced allergic contact dermatitis.

Attempts have been made to elucidate the immunopathogenesis of contact allergy; yet, the exact mechanism by which nickel-induced allergic contact dermatitis (NACD) occurs is far from clear and is discussed herein. It seems to suggest that a direct nickel-MHC class II molecule binding on the skin antigen presenting cells such as Langerhans cells (LCs) would result in Th1 cell activation. Substances such as serotonin and cytokines such as TNF-alpha produced by activated mast cells may increase adhesion molecule expression and thus, enhance T cell trafficking in the skin. Cytokines such as IFN-gamma and IL-1 and perhaps IL-12 certainly play a crucial role in the activation of Th1 cells. Along with possible function of CD8 cells, downregulation of NACD may be mediated by suppressed function of LCs via the action of activated keratinocytes-derived IL-10. Inhibition of NACD can also be generated by feeding with nickel, suggesting that the induction of oral tolerance to nickel may be beneficial for an alternative immunotherapy of nickel allergy. Nevertheless, this testable model provides a direction for further investigation.

The interleukin network in the immunopathogenesis of oral diseases.

Interleukins produced by both lymphoid and non-lymphoid cells play a crucial role in the immune response. This paper discusses the possible interleukin network in the immunopathogenesis of some oral diseases. In chronic inflammatory periodontal diseases and periapical inflammation, interleukins such as IL-1 and IL-6 may be responsible in tissue destruction. High levels of IL-12 but not IL-4 and IL-10 may reduce the course of candidal infection. The progression of HIV infection has been associated with the regulation of distinct cytokines; thus, the pathogenesis of Kaposi's sarcoma may be regulated by IL-6. In autoimmune-associated oral diseases such as lichen planus, the role of Langerhans cells in presenting autoantigens may parallel with increased levels of IL-6. It seems, therefore, that the course of these diseases is regulated by these polypeptides which may in turn modulate the disease severity. However, whether altered levels of interleukins in certain oral disorders can be used as a diagnostic marker requires further investigation.