The immune system protects the body from disease and infection. A fundamental aspect of this protection involves distinguishing between the body’s own components and foreign invaders. This ability relies on molecules known as self antigens, which act as unique identity markers for an individual’s cells and tissues. These markers allow the immune system to recognize what belongs to the body.
Understanding Self Antigens
Self antigens are molecules found on or within an individual’s own cells. These molecules can be proteins, carbohydrates, or lipids, and they are present on almost all cell types. For instance, red blood cells have specific self antigens on their surface that determine a person’s blood type, such as A, B, or O. Other examples include proteins on the surface of liver, colon, and thyroid cells.
Self antigens are distinct from “non-self” antigens, which originate from outside the body, such as those found on bacteria, viruses, or other foreign substances. The immune system is designed to identify these non-self antigens as potential threats and mount a response. Self antigens serve as a molecular “passport” that tells the immune system, “I belong here,” preventing it from attacking healthy tissues.
How the Immune System Recognizes Self
The immune system’s capacity to differentiate between self and non-self, and avoid attacking its own tissues, is known as immune tolerance. This recognition process is established through two primary phases during the development of immune cells. These phases ensure that immune cells do not react harmfully to the body’s own components.
The first phase, known as central tolerance, occurs as immune cells, specifically T cells in the thymus and B cells in the bone marrow, mature. During this period, these developing immune cells are “educated” to recognize and ignore self antigens. Any developing T or B cells that strongly react to self antigens are eliminated or inactivated through a process called negative selection, preventing them from circulating.
Even with central tolerance, some self-reactive immune cells may escape into circulation. Peripheral tolerance mechanisms then come into play. These additional safeguards suppress or inactivate any remaining self-reactive cells not removed during central tolerance. Regulatory T cells, for example, control and suppress these potentially harmful lymphocytes, ensuring they do not attack healthy tissues.
When Self-Recognition Goes Wrong
When the immune system’s self-recognition falters, it can lead to autoimmune diseases. In these disorders, the immune system mistakenly identifies self antigens as foreign invaders and attacks the body’s own healthy cells and tissues. This misdirected immune response results in inflammation and damage to various organs and systems.
The consequences of this breakdown can manifest in diverse ways, depending on which self antigens are targeted. For instance, in Type 1 Diabetes, the immune system attacks and destroys insulin-producing beta cells in the pancreas, leading to impaired blood sugar regulation. Another example is Rheumatoid Arthritis, where the immune system targets the lining of the joints, causing chronic inflammation, pain, and eventual joint damage.
Systemic Lupus Erythematosus, often referred to as Lupus, illustrates how widespread the impact can be, as the immune system can attack various organs and tissues, including the joints, skin, kidneys, and heart. These examples highlight that autoimmune diseases arise from a failure in the immune system’s ability to maintain tolerance to specific self antigens.