CD4+T Lymphocyte Subsets And Th1/Th2 Polarization In Oral Lichen Planus

Oral lichen planus (OLP) is a relatively common chronic inflammatory oral mucosal disease. The etiology and pathogenesis are still obscure. There are extensive data to suggest that OLP is a T cell-mediated immune damage. The histology of OLP is characterized by a dense subepithelial band-like infiltrate of T lymphocytes and by disruption of the epithelial basement membrane and degeneration of epithelial basal keratinocytes.Many studies have demonstrated that CD4+ T lymphocytes and their cytokines play a key role in the pathogenesis of immunologic diseases and orchestrating a specific mucosal immune response. The imbalance of T lymphocyte subsets might involve the pathogenesis of OLP. The CD4+ T cell has been divided into two further functional subsets, suppressor inducer subset (CD4+CD45RA+) and helper inducer subset (CD4+CD45RO+), by the expression of different isoform of the leucocyte common antigen (CD45). CD4+CD45RA+ T cells are important in the mature T lymphocyte-mediated immune response. They activate CD8+T cells to suppress Ig production. A decline in CD4+CD45RA+ T cells is a characteristic step in the development of autoimmune disorders because it implies a failure in the mechanisms of control of the immune response. T cell-mediated suppression plays a central role in the maintenance of self tolerance. A defect in T-suppressor circuits is implicated in the pathogenesis of autoimmune diseases.CD4+ T helper (Th) cells represent a functionally heterogeneous population. Th cells can be divided into different subsets based on their cytokine profile. ThO cells can further differentiate into Th1 or Th2 cells. The factors that may play a role in driving ThO cellsThe results indicate that Th2 immune response is predominant in OLP. A shift towards a Th2 cytokine may result in a defect in cell mediated immunity.Part III Regulation of BCG-polysaccharide nucleic acid and dexamethasone on Thl/Th2 cytokines in oral lichen planusPBMC were isolated from OLP patients and then stimulated with PHA, BCG-PSN and dexamethasone respectively for 72 hours (37C, 5% CO2). The concentrations of IFN- Y and IL-4 in culture supernatants were determined by ELISA. The mRNA levels for IFN- Y and IL-4 were examined in culture cells using semiquantitative RT-PCR. BCG-PSN increased significantly the levels of IFN-r, but had no effect on the production of IL-4. However, dexamethasone significantly inhibited the levels of IFN- Y and IL-4. IFN- Y production was inhibited significantly more than IL-4 by dexamethasone. BCG-PSN induces a switch from Th2 to Thl cytokine in OLP patients. Dexamethasone is a broad range immunosuppressant inhibiting Thl/Th2 cytokines. Both drugs have markedly different effect on cytokine production.