This time I would like to recommend you to read two review papers which provide a model for pathogenesis of oral autoimmune diseases.

When the aetiology to these diseases is discussed autoantibodies are often in focus although mechanistic understanding of autoimmune specificity may hinge on the identification of the full spectrum of disease relevant T cell epitopes.

The paper by Chow et al. (link to Pub Med abstract), addresses this issue and emphasise that it is likely that more than a single target antigen exists in a given autoimmune disease and that each antigen houses several epitopes. 

 

Increased appreciation of the key role of T lymphocytes in autoimmunity has led to exploration beyond traditional pan-immunosuppressive treatments that are the mainstay of autoimmune disease therapy.

Based on molecular and cellular T cell biology, there are several basic levels at which prevention and/or intervention might occur.

One of the most exciting techniques relates to “tolerizing” with peptide antigens to prevent the initiation of autoimmunity.

 

The second paper is published by Tan & O’Neill (link to PdF).
They give and interesting explanation to how the immune system can induce tolerance and immunity. External “danger signals” may through Toll-like receptors on activated dendritic cells, as Langerhan’s cells of oral epithelium, instigate autoimmunity if self-proteins are expressed to autoreactive T cells.

 

Together the two papers give a new insight to how autoimmunity may be orchestrated though professional antigen-presenting cells and auto-reactive T cells.