Selfantigen

Self-antigen refers to any molecule or epitope derived from the body's own proteins, lipids, or nucleic acids that can be recognized by the immune system. In a healthy individual, immune tolerance prevents responses against these self-components. T cells mature in the thymus with negative selection to remove strongly self-reactive clones, while B cells undergo similar processes in the bone marrow and periphery. Peripheral tolerance mechanisms, including regulatory T cells and anergy, further limit self-reactive responses.

When tolerance fails or is bypassed, self-antigens can become targets of the immune system, leading to autoimmunity. In that context, the antigens are often called autoantigens, and autoantibodies or autoreactive T cells directed against them characterize autoimmune diseases. Self-antigens may be tissue-specific or ubiquitous, and they are frequently presented as peptides bound to MHC molecules on the surface of cells.

Post-translational modifications, tissue injury, or infections can unmask or create new epitopes, sometimes triggering immune recognition of self. Molecular mimicry, where foreign antigens resemble self-antigens, is another proposed mechanism for initiating autoimmunity.

Examples of autoantigens include insulin and GAD65 in type 1 diabetes; myelin basic protein or proteolipid protein in multiple sclerosis; citrullinated proteins in rheumatoid arthritis; and nuclear antigens such as double-stranded DNA in systemic lupus erythematosus. Blood group antigens on red blood cells are inherited self-antigens that determine blood type but are not typically autoimmune targets. Alloantigens and neoantigens are related concepts describing non-self or modified self epitopes.