Topic overview

Start with the big picture

Self-tolerance is maintained through deletion of strongly self-reactive lymphocytes in the thymus and bone marrow, and through peripheral controls such as anergy, regulatory T cells, and immunological ignorance. Autoimmunity can emerge when these safeguards are impaired. Genetic susceptibility, including certain HLA class II alleles and regulatory gene variants, interacts with environmental triggers that may promote molecular mimicry, epitope spreading, or other forms of immune activation. Tissue injury commonly involves antibody-mediated effects, immune-complex deposition, or autoreactive T-cell responses. The disease examples illustrate how these pathways produce distinct patterns, including immune-complex nephritis in lupus, inflammatory joint damage in rheumatoid arthritis, receptor stimulation in Graves disease, and β-cell injury in type 1 diabetes. The full lesson develops these mechanisms alongside clinical features and consequences of chronic damage.