The expression of dual TCRs by the same T cell has been proposed to be a potential mechanism for autoimmune disease. Normally, high avidity self-reactive T cells are thymically depleted, but it has been hypothesized that the expression of a self-TCR on a T cell is lower when presented in the context of a second TCR, thereby providing a cover for high avidity self-TCRs from both central and peripheral tolerance. Blichfeldt et al. [62] demonstrated that dual tg-TCRs, which have lower expression of each TCR on the surface of a T cell, needed higher concentrations of peptide, presented by MHC, to induce a similar T cell proliferative response compared to a single receptor T cell.