Antigens are substances that trigger an immune response, designed to identify and neutralize foreign invaders. While many antigens come from outside the body, self-antigens are molecules within our own cells and tissues. The immune system normally recognizes these as belonging to the body. Correct recognition is important for health and prevents the immune system from attacking its own cells.
What Are Self-Antigens?
Self-antigens are molecules, including proteins, carbohydrates, and nucleic acids, naturally present on the surface or inside the body’s cells. Under healthy conditions, the immune system recognizes these as “self,” meaning they do not provoke an immune response. They serve as identifiers, labeling each cell as part of the individual.
Major Histocompatibility Complex (MHC) molecules are a prominent example, found on the surface of most cells, displaying protein fragments from inside the cell. These molecules are unique to each individual, similar to a cellular fingerprint, and play a role in immune recognition. Other examples include blood group antigens, carbohydrate molecules on red blood cells that determine blood type, and tissue-specific proteins like insulin in pancreatic cells.
How the Immune System Distinguishes Self
The immune system employs mechanisms to prevent attacking its own self-antigens, a process known as immune tolerance. One primary mechanism is central tolerance, occurring during immune cell development in specialized organs. T cells, for instance, mature in the thymus, and B cells develop in the bone marrow.
During this developmental stage, immature immune cells are exposed to many self-antigens. Cells that react too strongly are eliminated through apoptosis, or programmed cell death, or are rendered inactive. This “education” process ensures most self-reactive immune cells are purged before circulating throughout the body.
Beyond primary lymphoid organs, peripheral tolerance mechanisms further safeguard against autoimmunity. These processes inactivate or suppress self-reactive immune cells that may have escaped central tolerance. One mechanism is anergy, where self-reactive T cells become unresponsive upon encountering self-antigens without necessary co-stimulation signals. Additionally, specialized regulatory T cells (Tregs) actively suppress other immune cells that might attack self-antigens. These combined mechanisms maintain the immune system’s balance and prevent self-directed responses.
When the Immune System Attacks Self
When immune tolerance falters, the immune system can mistakenly identify self-antigens and attack the body’s own tissues. This misdirected response is known as autoimmunity, leading to a range of conditions called autoimmune diseases. In these diseases, the immune system’s protective function turns destructive, causing chronic inflammation and damage to various organs or systems.
For example, in Type 1 Diabetes, the immune system targets and destroys insulin-producing beta cells in the pancreas, which contain self-antigens. This destruction leads to an inability to produce insulin, resulting in high blood sugar levels. Similarly, Rheumatoid Arthritis involves the immune system attacking self-antigens in the lining of the joints, causing inflammation, pain, and eventual joint damage.
Multiple Sclerosis exemplifies another instance where the immune system attacks the myelin sheath, a fatty covering around nerve fibers in the brain and spinal cord, which contains self-antigens. This attack disrupts nerve signal transmission, leading to various neurological symptoms. These conditions underscore the profound consequences that arise when the immune system loses its ability to accurately distinguish between self and non-self, highlighting the ongoing importance of this recognition process for overall health.