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Hypersensitivity Reactions

Q: Which cells and immunoglobulins are involved in Type I hypersensitivity reactions?

Mast cells and basophils — the main effector cells with immunoglobulins fixed on their surface.IgE (immunoglobulin E) and less frequently IgG4 — the main immunogens driving the anaphylactic reaction.Type 2 T-helper cells (Th2) and antigen-presenting cells — participate in the immunological stage and the production of specific antibodies.

Q: Which specific mediators are released during the pathochemical stage of a Type I allergic reaction?

Histamine — a vasoactive amine released from granules of mast cells and basophils.Cysteinyl leukotrienes (LTC4, LTD4, LTE4) — lipid mediators that constitute the "slow-reacting substance of anaphylaxis".Prostaglandin D2 (PgD2) and platelet-activating factor (PAF) — mediators involved in bronchoconstriction and increased vascular permeability.Heparin — a proteoglycan stored in mast cell granules.

Q: What is the mechanism of target cell destruction in cytotoxic (Type II) hypersensitivity?

Interaction of antibodies of IgG and IgM classes with antigens that are components of the cell membrane or attached haptens.Activation of effector mechanisms (the complement system or killer cells) as a result of cell-antigen-antibody complex formation.Cytolysis — direct destruction of target cells driven by triggered immune mechanisms.

Q: What are haptens and why can they cause allergies?

Haptens (incomplete antigens) — low-molecular-weight compounds (less than 10 kDa) that cannot independently induce an immune response.Acquisition of immunogenicity — haptens become complete antigens after binding to the body's carrier proteins.Upon binding to a carrier protein, the hapten acquires the ability to induce an immune response and can participate in the development of an allergic reaction.

Q: What is the role of eosinophils in the late stages of immediate hypersensitivity?

Recruitment to the lesion — eosinophils are attracted by chemotactic factors and Th2 cytokines during the late phase of inflammation.Secretion of toxic proteins — they release major basic protein (MBP), eosinophil cationic protein (ECP), peroxidase, and leukotrienes.Tissue damage — these products cause direct injury and cytotoxicity to the airway epithelium, sustaining inflammation.

For medical students2 min readUpdated 2026-10-10

Hypersensitivity refers to a specific, inappropriate, and exaggerated immune response to a repeat encounter with an antigen (allergen). This process leads to damage of the body's own organs and tissues.

Onset speedImmediate: minutes to hours; Delayed: 24–72 hours.

Main mediatorsImmediate: antibodies (IgE, IgG, IgM); Delayed: macrophages and Th1 lymphocytes.

Common household triggerMites of the family Pyroglyphidae.

Stages of Allergic Reaction Development

An allergic response always proceeds through three consecutive phases:

Immune phase. Begins upon initial exposure to the antigen. Immunocompetent cells recognize the allergen and interact with it.
Pathochemical phase. Synthesis and release of cytokines and specific allergy mediators are triggered. Effector cells become activated.
Pathophysiological phase. Clinical manifestations of the reaction. These may affect the skin (itching, rashes), blood vessels (edema), or the respiratory system (asthma attacks).

Most commonly, allergies proceed via an IgE-dependent pathway, though other immune mechanisms are frequently involved.

Classification of Hypersensitivity Reactions

Historically, R. Cooke (1947) divided allergic reactions based on their onset speed into immediate hypersensitivity (IHS) and delayed-type hypersensitivity (DTH).

Later, in 1963, P. Gell and R. Coombs identified 4 main types of tissue injury in allergies. This classification remains foundational in modern immunology.

Gell-Coombs Type	Name	Key Players	Clinical Examples
Type I	Anaphylactic	IgE (less commonly IgG4)	Anaphylactic shock, pollinosis, urticaria, atopic asthma
Type II	Cytotoxic	IgG, IgM	Drug allergy, hemolytic anemia, leukopenia
Type III	Immune complex-mediated	IgG, IgM in complexes	Serum sickness, Arthus reaction, exogenous allergic alveolitis
Type IV	Cell-mediated (DTH)	Macrophages, $T_H1$	Contact dermatitis, graft rejection, infectious allergy

Comparison of Immediate and Delayed Hypersensitivity

Immediate hypersensitivity (IHS) is mediated by humoral immunity—IgE, IgG, and IgM antibodies (Types I, II, and III according to Gell and Coombs). The reaction develops rapidly: from a few minutes to a few hours after encountering the allergen. Vasodilation occurs, blood vessels become permeable, leading to itching, bronchospasm, and edema. Products of eosinophils and neutrophils are recruited during the late stages of IHS.

Delayed-type hypersensitivity (DTH) corresponds to Type IV in the Gell and Coombs classification and is mediated by cellular immunity. The antigen interacts directly with macrophages and Th1 lymphocytes, bypassing antibodies. The reaction develops 24–72 hours (1–3 days) after contact. Macrophages and T lymphocytes accumulate in the tissues, causing induration and local inflammation.

Etiology: Characteristics of Allergens

Allergens are antigens (mostly of protein nature with a molecular weight of 10–80 kDa). They are typically classified by their route of entry into the body into food, contact, parenteral (e.g., insect venom), and airborne.

Airborne allergens include fungal spores, animal dander, house dust mite particles (especially Pyroglyphidae, which are potent domestic allergens), and pollen.

Pollinic allergens exhibit pronounced seasonality and geographic distribution: trees bloom in spring, grasses in summer, and weeds at the end of summer into autumn. An important feature of pollen is its ability to cross-react due to structural similarities between its antigens and components of certain foods. A separate group of potent chemical allergens comprises drugs that act as haptens.

Frequently asked questions

Which cells and immunoglobulins are involved in Type I hypersensitivity reactions?

Mast cells and basophils — the main effector cells with immunoglobulins fixed on their surface.
IgE (immunoglobulin E) and less frequently IgG4 — the main immunogens driving the anaphylactic reaction.
Type 2 T-helper cells (Th2) and antigen-presenting cells — participate in the immunological stage and the production of specific antibodies.

Which specific mediators are released during the pathochemical stage of a Type I allergic reaction?

Histamine — a vasoactive amine released from granules of mast cells and basophils.
Cysteinyl leukotrienes (LTC4, LTD4, LTE4) — lipid mediators that constitute the "slow-reacting substance of anaphylaxis".
Prostaglandin D2 (PgD2) and platelet-activating factor (PAF) — mediators involved in bronchoconstriction and increased vascular permeability.
Heparin — a proteoglycan stored in mast cell granules.

What is the mechanism of target cell destruction in cytotoxic (Type II) hypersensitivity?

Interaction of antibodies of IgG and IgM classes with antigens that are components of the cell membrane or attached haptens.
Activation of effector mechanisms (the complement system or killer cells) as a result of cell-antigen-antibody complex formation.
Cytolysis — direct destruction of target cells driven by triggered immune mechanisms.

What are haptens and why can they cause allergies?

Haptens (incomplete antigens) — low-molecular-weight compounds (less than 10 kDa) that cannot independently induce an immune response.
Acquisition of immunogenicity — haptens become complete antigens after binding to the body's carrier proteins.
Upon binding to a carrier protein, the hapten acquires the ability to induce an immune response and can participate in the development of an allergic reaction.

What is the role of eosinophils in the late stages of immediate hypersensitivity?

Recruitment to the lesion — eosinophils are attracted by chemotactic factors and Th2 cytokines during the late phase of inflammation.
Secretion of toxic proteins — they release major basic protein (MBP), eosinophil cationic protein (ECP), peroxidase, and leukotrienes.
Tissue damage — these products cause direct injury and cytotoxicity to the airway epithelium, sustaining inflammation.

Which antibodies are involved in Type II and Type III reactions?

In both cases, IgG and IgM immunoglobulins play a key role. The difference is that in Type III, they function as part of circulating immune complexes.

How soon does delayed-type hypersensitivity manifest clinically?

Symptoms of DTH (Type IV) develop within 24 to 72 hours (1–3 days) after re-exposure to the allergen.

What is the role of T lymphocytes in allergies?

Type 1 T-helper cells ($T_H1$) and macrophages are the primary participants in delayed-type hypersensitivity (Type IV), providing a cell-mediated response and tissue infiltration.

Go deeper

Pathogenesis of anaphylactic shock
Mechanisms of immune complex formation (Type III)
Haptens: mechanisms of drug conversion into complete allergens
Features of cross-reactivity between pollen and food
Arthus phenomenon and serum sickness
Mechanisms of antireceptor reactions in cytotoxic hypersensitivity