Basic Properties and Completeness
To understand the mechanisms of immune defense, it is important to distinguish the basic characteristics of these molecules:
- Antigenicity — the potential ability to serve as a specific "stimulus" for immunocompetent cells.
- Immunogenicity — the ability to trigger a full-fledged protective response. It depends on molecular mass (strong immunogens are larger than 10 kDa), structure (heteropolymers with L-amino acids and soluble proteins work best), as well as the genetics and physiological background of the macroorganism.
- Foreignness — structural dissimilarity from the organism's own tissues.
- Specificity — the uniqueness of the structure that determines the precise direction of the response.
Based on their ability to elicit a reaction, substances are divided into two groups:
- Complete antigens. These possess a large mass and a complex structure. They independently initiate an immune response and bind to its products.
- Haptens (incomplete antigens). Low-molecular-weight substances (e.g., oligopeptides). By themselves, they do not elicit a response, but if they bind to a large carrier protein within the body, they acquire the properties of complete antigens.
Structural Organization: Epitopes
Antigen specificity is determined by epitopes (antigenic determinants)—small characteristic regions that directly contact receptors of the immune system cells. A single antigen may carry multiple different epitopes.
- Linear epitopes consist of a continuous chain of 6–12 amino acids. They are recognized by both B lymphocytes and T lymphocytes (for presentation to T helper cells, the epitope length can reach up to 25 residues).
- Conformational epitopes are formed during the spatial folding of a molecule when distant parts of the chain are brought into close proximity. Such determinants are "seen" only by B lymphocytes and antibodies. Any protein denaturation leads to the destruction of the spatial structure and the loss of the original determinants.
A mutation and substitution of just a single amino acid can lead to the formation of a molecule with fundamentally new properties. Vaccine prophylaxis often relies on the addition of adjuvants—substances that nonspecifically enhance the immunogenicity of administered antigens.
Microbial Antigens and Mimicry
A bacterial cell contains a whole set of antigens, knowledge of which allows for the precise identification of the pathogen and the creation of vaccines:
- O-antigen (somatic). Associated with the lipopolysaccharide (LPS) of the outer membrane of Gram-negative bacteria. Noted for its thermostability (withstands boiling).
- H-antigen (flagellar). Consists of the flagellin protein. Thermolabile (destroyed at 56–80 °C).
- K-antigen (capsular). Most often polysaccharide in nature. Interaction with a specific serum causes a visible "capsular swelling" phenomenon. Its variant—the Vi-antigen—is a marker of high virulence.
Many microbes secrete exotoxins—protein antigens. If they are chemically stripped of toxicity while retaining immunogenicity, toxoids (anatoxins) are formed (the basis for vaccines).
Sometimes microbes form structures resembling normal human tissues. This is called antigenic mimicry. For example, the M-protein of hemolytic streptococcus shares similarities with myocardial and glomerular antigens. During infection, the immune system begins to cross-attack its own cells, leading to rheumatic fever or post-streptococcal glomerulonephritis.
Erythrocyte Antigens (Blood Groups)
Over 200 allogeneic antigens are located on erythrocyte membranes. Clinically, the most significant are the AB0 and Rh (rhesus factor) systems.
The AB0 system is based on the baseline H antigen, from which antigens A and B are synthesized. Their combination determines the blood group (e.g., blood type O lacks antigens A and B, whereas blood type AB possesses both). If incompatible blood is transfused, antibodies attack the foreign erythrocytes. Agglutination and intravascular hemolysis develop, leading to severe hemolytic shock.
Rhesus incompatibility often occurs during pregnancy if the mother is Rh-negative and the fetus is Rh-positive. The mother's immune system produces antibodies that destroy the child's red blood cells, causing neonatal jaundice syndrome.