We have documented a universal state of ‘benign’ autoimmunity imprinted in all individuals, characterized by a similar frequency and naïve-like phenotype of circulating autoreactive CD8⁺ T cells irrespective of disease status. Our aim is to identify biomarkers distinguishing benign versus pathogenic autoimmune T cells, and the mechanisms of their transition from one state to another. Mechanisms under consideration include the role of initiating environmental triggers (e.g. Coxsackievirus infections), T-cell cross-reactivity, and resistance to apoptosis/exhaustion.