Historical Aspects and Theory Development
The understanding of the connection between the body's protective reactions has evolved over centuries. A major milestone was the establishment of the phagocytic theory by É. Metchnikoff, which laid the foundations of cellular immunity. In 1908, É. Metchnikoff and P. Ehrlich, the author of the humoral immunity theory, were awarded the Nobel Prize, and Metchnikoff first demonstrated the adaptive nature of inflammation.
In the 20th century, the relationship between inflammation, reactivity, and allergy was actively studied. In 1907, C. Pirquet proposed using hyperergic reactions for diagnostics. Later, in 1914, R. Rössle established that exudative inflammation underlies such processes, terming it hyperergic. By the mid-20th century, the concepts of inflammation and immunity converged, and academician A.I. Strukov formulated the concept of immune inflammation.
Biological Purpose and Interaction Mechanisms
Immunity and inflammation share a common goal: clearing the body of pathogenic irritants, foreign factors, necrotic tissues, and immune complexes. The interaction of these processes is realized through a bidirectional link:
- Inflammation triggers immunity: tissue damage and the development of an inflammatory response release antigenic structures that stimulate immune mechanisms.
- Immunity is realized through inflammation: effective immune defense can prevent the development of inflammation, but in hypersensitivity reactions, inflammation acts as their direct morphological manifestation. If the triggering mechanism is an immune system reaction, immune inflammation develops.
Concept of the Unified Defense System
According to V.S. Paukov's concept, inflammation and immunity function as an inseparable system divided into sequential stages:
- Immediate non-specific reactions (inflammation): ensure pathogen isolation, primary destruction, and containment of aggression. Phagocytosis of microorganisms allows the identification of antigenic determinants and the transmission of information to immunocompetent organs.
- Subsequent specific reactions (immunity): unfold on average within 10–14 days. During this period, B-lymphocytes transform into plasma cells, specific immunoglobulins are synthesized, and T-lymphocytes undergo hyperplasia.
Subsequent specific defense is also realized through inflammatory mechanisms, and final tissue repair occurs via the productive phase of the inflammatory process.
Influence of Immune Status on the Character of Inflammation
The clinical picture and outcome of an inflammatory reaction directly depend on the state of the immune system. Defects in its individual links can radically alter the course of the process.
With a pronounced deficiency of T-lymphocytes (observed in nude mice or humans with primary immunodeficiencies such as DiGeorge, Wiskott-Aldrich, and Ataxia-Telangiectasia syndromes), the body's ability to form a full-fledged restrictive response against pyogenic microorganisms is impaired. This leads to severe consequences: generalized infection, sepsis, and death.