Place in the pathology of the immune system
Contact with an antigen does not always end with a protective response alone—sometimes mechanisms are triggered that damage the body's own tissues. Such conditions are called hypersensitivity reactions.
They are divided into 4 types depending on the immunological mechanism. While type II is associated with cytotoxic antibodies, type III with immune complexes, and type IV with the cellular response of lymphocytes, type I is characterized by the rapid release of spasmogenic and vasoactive substances.
Pathogenesis: from contact to degranulation
The development of anaphylactic reactions is based on the interaction of the allergen with IgE antibodies. The process occurs in several stages:
- Primary contact: the antigen enters the body, activating B lymphocytes, which begin to synthesize IgE.
- Sensitization: IgE molecules firmly bind via their Fc fragment to receptors on the surface of mast cells and basophils.
- Re-exposure: the allergen cross-links IgE molecules on the surface of the already sensitized mast cell.
- Activation and degranulation: the cell releases primary mediators and begins the synthesis of secondary mediators de novo (from arachidonic acid metabolites).
Interestingly, mast cells can also be activated without the involvement of antigens. Triggers can include complement system anaphylatoxins (C3a and C5a), macrophage cytokines (IL-8), physical factors (heat, cold, solar radiation), and even certain drugs (morphine, codeine).
Two phases of the allergic response
The immediate-type reaction unfolds over time and has two distinct stages, differing in mediators and clinical effects.
Early phase Begins 5–30 minutes after exposure to the allergen. The main sources of mediators here are basophils and mast cells, which release histamine and leukotrienes. This leads to vasodilation, increased vascular permeability, mucosal edema, hypersecretion of mucus, and smooth muscle spasm.
Late phase Starts 2–8 hours later even without re-exposure to the antigen and can last for several days. Under the influence of platelet-activating factor (PAF) and tumor necrosis factor-alpha (TNF-α), inflammatory cells are recruited to the tissue: monocytes, neutrophils, basophils, and, most importantly, eosinophils. The outcome of this phase is damage to epithelial cells.
The role of eosinophils
Eosinophils are key players in the late phase. They possess a wide spectrum of mediators similar to mast cells, but additionally secrete specific toxic proteins:
- MBP (Major Basic Protein) — major basic protein;
- ECP (Eosinophil Cationic Protein) — eosinophil cationic protein.
Under normal conditions, these proteins are vital for the destruction of parasites and microorganisms. However, in pathology (e.g., in bronchial asthma), their aggressive action is directed against the body's own tissues, causing destruction of the airway epithelium.
Clinical forms: systemic and local
The manifestations of type I hypersensitivity depend on the route of antigen entry and the degree of sensitization of the body.
Systemic anaphylaxis Most commonly occurs upon intravenous administration of an allergen (heterologous proteins, polysaccharides, penicillin). Anaphylactic shock develops, the severity of which directly depends on the level of prior sensitization. At the same time, the shock dose of the antigen can be infinitesimally small.
Local anaphylaxis (atopic allergy) Occurs in one-tenth of the population and has a pronounced familial predisposition. It arises in response to exogenous allergens: house dust, pollen, animal dander, food. Manifestations depend on the site of contact:
- Skin: urticaria, angioedema (Quincke's edema);
- Mucous membranes: allergic rhinitis (hay fever), conjunctivitis;
- Respiratory tract: bronchial asthma;
- Gastrointestinal tract: food allergy (allergic gastroenteritis).
To remember the pathogenesis of type I, use the "SAD" rule: Sensitization (IgE fixation), Activation (allergen binding to IgE), Degranulation (release of mediators by mast cells).
Class and exam questions
Can mast cell degranulation occur without the involvement of an allergen?
Yes, activation can be caused by complement anaphylatoxins (C3a, C5a), interleukin-8, physical factors (cold, heat, solar radiation), and certain drugs, such as morphine or codeine.
Why is the epithelium damaged in bronchial asthma?
This is a consequence of the late phase of the reaction. Eosinophils migrate into the tissue and release aggressive proteins—MBP and ECP. Normally they kill parasites, but in asthma, they destroy the cells of the mucosa.
What determines the severity of systemic anaphylactic shock?
The severity of the reaction correlates with the level of prior sensitization of the body (the amount of accumulated IgE). With high sensitization, even an exceptionally small dose of antigen can become a shock dose.
What else to study on this topic
- Differences between type I hypersensitivity and types II, III, and IV
- Mechanisms of synthesis of secondary mediators from arachidonic acid
- Pathogenesis and morphology of anaphylactic shock
- Genetic factors in the development of atopic allergy
- The role of the complement system in non-immune mast cell activation
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