Selbstantigene

Selbstantigene, sometimes written as Selbstantigene, are antigens derived from the body's own proteins and tissues that can be recognized by the immune system. In immunology they are contrasted with non-self antigens such as those from pathogens, vaccines, or transplanted tissues. The study of Selbstantigene focuses on how the immune system distinguishes self from non-self and how this distinction can fail in autoimmunity.

Central and peripheral tolerance are key mechanisms that prevent immune responses against Selbstantigene. During early lymphocyte development in the thymus and bone marrow, self-reactive cells are deleted or inactivated. In mature life, peripheral tolerance uses regulatory T cells, anergy, and other controls to restrain autoreactive cells that escape central tolerance.

Self-antigens can be categorized by distribution and accessibility. Tissue-restricted self-antigens are expressed mainly in specific organs, such as insulin in the pancreas or myelin proteins in the nervous system. Ubiquitous self-antigens are present in many tissues. Some self-antigens are sequestered behind barriers (for example in the eye or brain) and may become exposed after trauma or inflammation, potentially triggering autoimmune responses.

Autoimmunity can arise when tolerance is breached by genetic predisposition, environmental triggers, infections, or molecular mimicry, where pathogen-derived antigens resemble self-antigens. Autoreactive T cells and autoantibodies target Selbstantigene, contributing to diseases such as systemic lupus erythematosus, type 1 diabetes, rheumatoid arthritis, and multiple sclerosis. Modified or neoantigens, formed by processes like citrullination or oxidation, can also become immunogenic.

In clinical practice, detecting autoantibodies against Selbstantigene assists diagnosis and monitoring, while therapies often aim to dampen autoreactive responses or restore tolerance.