The self-organized criticality theory explains that systemic autoimmunity, or systemic lupus erythematosus (SLE), necessarily takes place when host’s immune system is overstimulated by repeated exposure to antigen, i.e., external disturbance, to levels that surpass the immune system’s stability-limit, i.e., self-organized criticality. The autoreactive lymphocyte clones, which we name autoantibody-inducing CD4 T (aiCD4 T) cells, are newly generated via de novo T cell receptor (TCR) revision from thymus-passed non-autoreactive clones at peripheral lymphoid organs. They not only stimulate B cells to generate varieties of autoantibodies but also help final differentiation of CD8 T cell into cytotoxic T lymphocyte (CTL) via antigen cross-presentation to induce tissue injuries identical to SLE. The causative antigen can be individually different, but such antigen must first be correctly presented to T cells and subsequently overdrive the person’s CD4 T cells in relation to his/her HLA to generate aiCD4 T cells. The ability of a certain antigen to cause autoimmunity depends on its propensity to be presented and/or cross-presented effectively, resulting in the overstimulation of CD4 and/or CD8 T cells of certain host beyond critical limit, i.e., self-organized criticality.
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