Many individuals carry low‑affinity self‑reactive

lymphocytes that escape deletion but remain functionally silent under normal

conditions due to intact immune tolerance mechanisms. Epidemiological studies

show that autoimmune diseases often arise after infections, tissue injury, or

chronic inflammation—even in individuals without identifiable monogenic defects

in immune regulation. In many cases, disease persists long after the initiating

inflammatory event has resolved.

What is the most plausible explanation for how inflammatory

environments contribute to the initiation of autoimmune disease?