Immune System Alterations
The development of immune inflammation is always accompanied by profound systemic shifts. In the humoral arm, a pronounced immunoglobulin imbalance comes to the forefront. Alterations occur in the normal concentrations of IgA, IgG, and IgM in peripheral blood, while their tissue levels increase pathologically. Concurrently, elevated concentrations of circulating immune complexes (CICs) are registered in blood and tissue structures.
Cellular immunity also undergoes a series of adverse changes. Laboratory tests reveal lymphopenia and an overall reduction in the T-lymphocyte population. The deficit affects specific subpopulations: the levels of both T helper cells and T suppressor cells drop. This leads to an imbalance in the immunoregulatory index — disrupting the critically important ratio between helpers and suppressors. Additionally, a decrease in leukocyte chemotactic activity is recorded, which directly impacts their ability to migrate to the lesion site.
Morphogenesis of Inflammation in Immediate Hypersensitivity
In immediate hypersensitivity reactions (Type I/III reactions) and various immune complex diseases (such as anaphylaxis), morphogenesis proceeds in a strict sequence. This cascade includes six key stages:
- Formation of immune precipitates. Insoluble antigen-antibody complexes form within the blood vessel lumen. Localization depends on the type of pathology: in the Arthus reaction, precipitates settle predominantly in venules, whereas in systemic immune complex diseases, they settle in arteries.
- Complement fixation. The formed immune complexes actively bind complement system factors.
- Chemotaxis. Polymorphonuclear leukocytes are recruited to the formed precipitates. They accumulate in large numbers both within the walls of affected vessels and perivascularly.
- Degranulation. Recruited leukocytes release aggressive lysosomal enzymes. Simultaneously, potent vasoactive substances are generated.
- Phagocytosis. Leukocytes begin to engulf and intracellularly digest the deposited immune complexes.
- Vascular wall injury. Under the destructive action of vasoactive substances, fibrinoid necrosis of the vessel wall develops. The process is accompanied by marked surrounding tissue edema and perivascular hemorrhages.
Outcome: A severe exudative-necrotic reaction forms in the affected zone, typically characterized by the appearance of a serous-hemorrhagic exudate.
Specifics of the Inflammatory Response in Delayed-Type Hypersensitivity
Delayed-type hypersensitivity (DTH), of which the tuberculin reaction is a classic example, has a fundamentally different morphological pattern and is characterized by a protracted course.
Unlike immediate hypersensitivity where polymorphonuclear leukocytes predominate (here they are virtually absent or extremely sparse), the primary effector role in DTH belongs to T-lymphocytes and macrophages. The mechanism of injury involves these immunocompetent cells independently finding the target antigen directly within the tissue and destroying it along with the tissue itself.
Microcirculatory disturbances in this type of reaction are weakly expressed. A specific cellular infiltrate forms within the conflict zone, consisting of lymphocytes, macrophages, and frequently, giant cells. Based on morphological features, this inflammation is classified as productive (granulomatous), or less commonly, interstitial inflammation.