Immune system disorders
The development of immune inflammation is always accompanied by profound systemic shifts. In the humoral link, a pronounced immunoglobulin imbalance comes to the fore. There is a change in the normal concentration of IgA, IgG, and IgM antibodies in the peripheral blood, while their tissue levels increase pathologically. Simultaneously, an elevated concentration of circulating immune complexes (CICs) is recorded in the blood and tissue structures.
Cellular immunity also undergoes a number of negative changes. Laboratory tests show lymphocytopenia and a general decrease in the T-lymphocyte population. The deficit affects specific subpopulations: the levels of both T-helper 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 the chemotactic activity of leukocytes is recorded, which directly impairs their ability to migrate to the lesion site.
Morphogenesis of inflammation in immediate hypersensitivity
In immediate-type hypersensitivity reactions (ITH) and various immune complex diseases (e.g., 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 phenomenon, precipitates settle predominantly in venules, whereas in systemic immune complex diseases, they settle in arteries.
- Complement binding. The formed immune complexes actively bind complement system factors.
- Chemotaxis. Polymorphonuclear leukocytes are attracted to the formed precipitates. They accumulate in large numbers both within the walls of the affected vessels and perivascularly.
- Degranulation. The attracted leukocytes release aggressive lysosomal enzymes. Concurrently, potent vasoactive substances are generated.
- Phagocytosis. Leukocytes begin to engulf and intracellularly digest the deposited immune complexes.
- Vascular wall damage. Under the destructive action of vasoactive substances, fibrinoid necrosis of the vascular wall develops. The process is accompanied by marked surrounding tissue edema and perivascular hemorrhage.
Outcome: A severe exudative-necrotic reaction forms in the affected area, typically characterized by the appearance of serous-hemorrhagic exudate.
Specifics of the inflammatory reaction in delayed-type hypersensitivity
Delayed-type hypersensitivity (DTH), a classic example of which is the tuberculin reaction, presents a fundamentally different morphological picture and is characterized by a protracted course.
Unlike ITH, where polymorphonuclear leukocytes predominate (here they are practically absent or extremely sparse), the main effector role in DTH belongs to T-lymphocytes and macrophages. The mechanism of damage is that these immunocompetent cells independently find the target antigen directly within the tissue and destroy it along with the tissue itself.
Microcirculatory disturbances in this type of reaction are poorly expressed. A specific cellular infiltrate consisting of lymphocytes, macrophages, and frequently giant cells forms in the conflict zone. Based on morphological features, this inflammation is classified as productive (granulomatous), or somewhat less frequently, as interstitial inflammation.
Briefly: answers to topical questions
Which disorders are classified as systemic immune complex diseases?
Systemic immune complex diseases include pathologies in which immune complexes form in the blood or lymph and become fixed in various organs, most frequently settling within the vascular bed. This group includes the following conditions:
- Acute serum sickness — occurs following repeated administration of large quantities of foreign serum.
- Chronic serum sickness — develops with persistent antigenemia and prolonged contact with the antigen.
- Rheumatoid arthritis — a disease with a frequently unidentified antigen.
- Polyarteritis nodosa — proceeds with vascular involvement.
- Membranous nephropathy — a pathology with an unknown antigen.
- Certain vasculitides.
What are the types of hypersensitivity reactions according to the Gell and Coombs classification?
According to the Gell and Coombs classification, there are four main types of hypersensitivity reactions based on different immunological mechanisms.
- Type I (anaphylactic) — characterized by the release of vasoactive and spasmogenic substances.
- Type II (cytotoxic) — associated with the involvement of antibodies in cell damage, promoting their phagocytosis or lysis.
- Type III (immune complex) — driven by the interaction of antigen and antibody with the formation of immune complexes that activate complement.
- Type IV (cell-mediated or delayed) — represents a cellular immune response involving sensitized lymphocytes, in which the antigen interacts with macrophages and Th1 lymphocytes.
For quick memorization of the differences, use the contrast rule: ITH involves vessels (venules/arteries), polymorphonuclear leukocytes, and rapid necrosis with exudate. DTH involves tissue, T-lymphocytes with macrophages, and protracted productive inflammation (granulomas).
Class and exam questions
What is the triggering mechanism for the development of immune inflammation?
The process is initiated by direct tissue damage. The main damaging factors are circulating immune complexes (consisting of antigen and antibody), the activated complement system, and various immune mediators.
Which pathologies belong to immediate-type hypersensitivity reactions (ITH)?
Immediate-type reactions include anaphylaxis (anaphylactic reaction) and the Arthus phenomenon. They are characterized by the rapid development of exudative-necrotic changes in blood vessels.
How does the cellular composition change during cellular immunity disorders?
Marked lymphocytopenia is observed with a decrease in the overall T-lymphocyte population. The levels of T-helpers and T-suppressors also drop, leading to an imbalance in the immunoregulatory index and a decrease in the chemotactic activity of leukocytes.
What type of inflammation is characteristic of DTH?
In delayed-type hypersensitivity, productive (granulomatous) or, somewhat less frequently, interstitial inflammation develops with the formation of an infiltrate composed of lymphocytes and macrophages.
What else to study on this topic
- Mechanisms of formation and circulation of circulating immune complexes (CICs).
- The role of lysosomal enzymes and vasoactive substances in the degranulation process.
- Differences in the localization of precipitates in the Arthus phenomenon versus systemic immune complex diseases.
- Morphological picture of fibrinoid necrosis of the vascular wall.
- Cellular composition of the infiltrate in DTH: functions of macrophages and giant cells.
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