Historical aspects and development of the theory
Understanding the connection between the body's defense reactions has evolved over centuries. A major milestone was the establishment of the phagocytic theory by I.I. Metchnikoff, which laid the foundations of cellular immunity. In 1908, I.I. Metchnikoff and P. Ehrlich, the author of the humoral immunity theory, were awarded the Nobel Prize, and Metchnikoff demonstrated the adaptive nature of inflammation for the first time.
In the 20th century, the relationship between inflammation, reactivity, and allergy was actively studied. In 1907, C. Pirquet proposed using the hyperergic reaction 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 between 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 mediated through inflammation: an 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 a 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): provide pathogen isolation, initial destruction, and containment of aggression. Phagocytosis of microorganisms allows for the identification of antigenic determinants and the transmission of information to immunocompetent organs.
- Subsequent specific reactions (immunity): unfold on average over 10–14 days. During this period, B lymphocytes transform into plasmacytes, specific immunoglobulins are synthesized, and T lymphocytes undergo hyperplasia.
Subsequent specific defense is also implemented through inflammatory mechanisms, while final tissue repair occurs via the productive phase of the inflammatory process.
Influence of immune status on the nature of inflammation
The clinical presentation and outcome of an inflammatory reaction directly depend on the state of the immune system. Defects in its individual components can radically alter the course of the process.
With marked T-lymphocyte deficiency (observed in nude mice or humans with congenital immunodeficiencies such as DiGeorge, Wiskott-Aldrich, and Louis-Bar syndromes), the body's ability to form a full-fledged restrictive response to pyogenic microorganisms is impaired. This leads to severe consequences: generalized infection, sepsis, and death.
Briefly: answers to topical questions
What morphological signs are characteristic of hyperergic inflammation?
Hyperergic inflammation is characterized by exudative-necrotic changes in vessel walls and pronounced cellular reactions. The main morphological features include:
- Exudative inflammation — underlies hyperergic reactions.
- Vasculitis — accompanied by fibrinoid necrosis of small vessel walls and hemorrhages.
- Cellular infiltration — manifested by moderate lymphocyte proliferation, as well as neutrophil infiltration of the spleen and lymph nodes.
Which cells present antigens to immunocompetent cells in the focus of inflammation?
Antigen presentation to immunocompetent cells in the inflammatory focus is carried out by specialized antigen-presenting cells, primarily macrophages and B lymphocytes.
- Macrophages — are the first to detect foreign antigens, perform non-specific uptake, and present them to the immune system.
- B lymphocytes — are responsible for specific antigen recognition.
The action of these cells involves processing the antigen and displaying its peptides on the cell membrane for subsequent interaction with T helper cells.
Which classes of immunoglobulins are synthesized by plasmacytes in the focus of immune inflammation?
The sources explicitly indicate the following immunoglobulins associated with plasmacytes and immune reactions:
- Immunoglobulin A (IgA) — mature plasmacytes in the lamina propria of the mucosa secrete IgA.
- Immunoglobulin E (IgE) — during sensitization in type I hypersensitivity reactions, B cells differentiate into plasma cells, after which IgE antibodies are synthesized.
- Immunoglobulins G and M (IgG, IgM) — participate in type II cytotoxic hypersensitivity reactions and type III immune complex reactions.
Which inflammatory mediators are released during immediate-type hypersensitivity reactions?
During immediate-type hypersensitivity reactions, primary and secondary inflammatory mediators are released, determining the early and late phases of the process.
- Histamine and leukotrienes — the main mediators of the early phase, causing edema, hypersecretion of mucus, and smooth muscle spasm.
- Platelet-activating factor (PAF) and tumor necrosis factor-alpha (TNF-α) — late-phase mediators that recruit inflammatory cells.
- Major basic protein (MBP) and eosinophil cationic protein (ECP) — specific eosinophil proteins capable of causing epithelial damage.
What is the difference between cellular and humoral immunity in the mechanisms implementing the inflammatory reaction?
The difference between cellular and humoral immunity lies in the leading mechanisms and cells that implement the inflammatory reaction.
| Characteristic | Cellular immunity | Humoral immunity |
|---|---|---|
| Basis of the reaction | Phagocytosis and specific interaction of T lymphocytes with antigen | Action of antibodies and immune complexes |
| Key cells | Type 1 T helpers (Th1), cytotoxic T lymphocytes (CD8+), macrophages | Type 2 T helpers (Th2), B lymphocytes, plasmacytes |
| Type of response | Cytokine response (more pronounced inflammation) | Antibody response (immunoglobulin synthesis) |
| Association with hypersensitivity | Delayed-type hypersensitivity (DTH) | Immediate-type hypersensitivity (ITH), cytotoxic and immune complex reactions |
Class and exam questions
What is the general biological meaning of inflammation and immunity?
Their common goal is to clear the body of pathogenic irritants, foreign factors, or altered native tissues, as well as to reject the damaging agent and subsequently restore (repair) them.
What is immune inflammation?
This is a special type of inflammation that develops when the cause and initiation of the process stem from a direct reaction of the immune system.
What are the consequences of T-lymphocyte defects in inflammation?
The absence of a full-fledged restrictive inflammatory response to pyogenic microorganisms in T-cell deficiency leads to generalized infection, the development of sepsis, and potentially death.
What else to study on this topic
- I.I. Metchnikoff's phagocytic theory and cellular immunity
- P. Ehrlich's theory of humoral immunity
- Arthus phenomenon and hyperergic inflammation
- Congenital immunodeficiency syndromes (DiGeorge, Wiskott-Aldrich, ataxia-telangiectasia)
- The role of non-specific and specific reactions in the unified defense system
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