Type I hypersensitivity

Type I hypersensitivity
Other names	Immediate hypersensitivity

Image showing the mechanism of activation of type 1 hypersensitivity in a mast cell.
Specialty	Immunology

Type I hypersensitivity (or immediate hypersensitivity), in the Gell and Coombs classification of allergic reactions, is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen.^[1] Type I is distinct from type II, type III and type IV hypersensitivities. The relevance of the Gell and Coombs classification of allergic reactions has been questioned in the modern-day understanding of allergy, and it has limited utility in clinical practice.^[2]

Exposure may be by ingestion, inhalation, injection, or direct contact.

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Pathophysiology

In type I hypersensitivity, B cells are stimulated (by CD4⁺ T_h2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM. During sensitization, the IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils.^[3] Mast cells and basophils coated by IgE antibodies are "sensitized". Later exposure to the same allergen cross-links the bound IgE on sensitized cells, resulting in anaphylactic degranulation, which is the immediate and explosive release of pharmacologically active pre-formed mediators from storage granules and concurrent synthesis of inflammatory lipid mediators from arachidonic acid;^[4] some of these mediators include histamine, leukotriene (LTC4 and LTD4 and LTB4), and prostaglandin, which act on proteins (e.g., G-protein coupled receptors) located on surrounding tissues.^[4] The principal effects of these products are vasodilation and smooth-muscle contraction.

Type I hypersensitivity can be further classified into immediate and late-phase reactions. Within minutes of exposure to an antigen, the immediate hypersensitivity occurs, releasing histamines and lipid mediators which are responsible for the initial allergic reaction response. However, about 4-12 hours after antigen exposure, a cough and wheezing may persist in the patient, along with swelling and redness of the skin. This is known as the late-phase hypersensitivity reaction which can last from approximately 1-3 days and is caused by the release of additional mediators from the mast cells and basophils.^[5]

List of a few mediators released by mast cells in type 1 hypersensitivity and their actions
Vasodilation and increased permeability	Histamine PAF Leukotriene C4, D4, and E4 Prostaglandin D2 Neutral proteases
Smooth muscle spasm	Histamine PAF Leukotriene C4, D4, and E4 Prostaglandin
Leukocyte extravasation	Cytokines (e.g. chemokines and TNF) Leukotriene B4 Chemotactic factors for neutrophils and eosinophils
Unless otherwise specified, the reference for this table is:^[6]

The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock.

Treatment and prognosis

If multiple systems are involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal.

Treatment usually involves adrenaline (epinephrine) because it counteracts anaphylaxis by increasing blood flow and relaxing bronchial muscles that block one’s airways.^[7] Antihistamines and corticosteroids are also commonly used in less severe reactions.^[8]

Examples

Some examples:

References

^ med/1101 at eMedicine
^ Descotes, Jacques; Choquet-Kastylevsky, Geneviève (February 2001). "Gell and Coombs's classification: is it still valid?". Toxicology. 158 (1–2): 43–49. doi:10.1016/S0300-483X(00)00400-5. PMID 11164991.
^ "The Adaptive Immune System: Type I Immediate Hypersensitivity". Archived from the original on 2010-07-27. Retrieved 2008-09-22.
^ ^a ^b Moon TC, Befus AD, Kulka M (2014). "Mast cell mediators: their differential release and the secretory pathways involved". Front Immunol. 5: 569. doi:10.3389/fimmu.2014.00569. PMC 4231949. PMID 25452755. This release of pre-formed mediators enables not only rapid anaphylactic reactions and allergic responses but also initiates recruitment of leukocytes to sites of pathogen invasion, activation of innate immune processes, and inflammatory responses (1). ... Two types of degranulation have been described for MC: piecemeal degranulation (PMD) and anaphylactic degranulation (AND) (Figures 1 and 2). Both PMD and AND occur in vivo, ex vivo, and in vitro in MC in human (78–82), mouse (83), and rat (84). PMD is selective release of portions of the granule contents, without granule-to-granule and/or granule-to-plasma membrane fusions. ... In contrast to PMD, AND is the explosive release of granule contents or entire granules to the outside of cells after granule-to-granule and/or granule-to-plasma membrane fusions (Figures 1 and 2). Ultrastructural studies show that AND starts with granule swelling and matrix alteration after appropriate stimulation (e.g., FcεRI-crosslinking).
Figure 1: Mediator release from mast cells
Figure 2: Model of genesis of mast cell secretory granules
Figure 3: Lipid body biogenesis
Table 2: Stimuli-selective mediator release from mast cells
^ Abbas, Malak; Moussa, Mohamed; Akel, Hassan (2024), "Type I Hypersensitivity Reaction", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 32809396, retrieved 2024-03-15
^ Table 5-2 in:Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 978-1-4160-2973-1. 8th edition.
^ Kemp, S. F., Lockey, R. F., Simons, F. E., & World Allergy Organization ad hoc Committee on Epinephrine in Anaphylaxis (2008). Epinephrine: the drug of choice for anaphylaxis-a statement of the world allergy organization. The World Allergy Organization journal, 1(7 Suppl), S18–S26. https://doi.org/10.1097/WOX.0b013e31817c9338. “The β-adrenergic properties of epinephrine cause bronchodilation… Epinephrine administration enhances coronary blood flow…”
^ "Recognizing and Treating Reaction Symptoms - FoodAllergy.org". www.foodallergy.org. Retrieved 2024-03-15.

External links

Hypersensitivity and autoimmune diseases

Type I/allergy/atopy
(IgE)

Foreign	Atopic dermatitis Allergic urticaria Allergic rhinitis (Hay fever) Allergic asthma Anaphylaxis Food allergy common allergies include: Milk Egg Peanut Tree nut Seafood Soy Wheat Penicillin allergy
Autoimmune	Autoimmune urticaria Eosinophilic esophagitis

Type II/ADCC

- IgM
- IgG

Foreign

Hemolytic disease of the newborn

Autoimmune

Cytotoxic	Autoimmune hemolytic anemia Immune thrombocytopenic purpura Bullous pemphigoid Pemphigus vulgaris Rheumatic fever Goodpasture syndrome Guillain–Barré syndrome
"Type V"/receptor	Graves' disease Myasthenia gravis Pernicious anemia

Type III
(Immune complex)

Foreign	Henoch–Schönlein purpura Hypersensitivity vasculitis Reactive arthritis Farmer's lung Post-streptococcal glomerulonephritis Serum sickness Arthus reaction
Autoimmune	Lupus Subacute bacterial endocarditis Rheumatoid arthritis

Type IV/cell-mediated
(T cells)

Foreign	Allergic contact dermatitis Mantoux test
Autoimmune	Type 1 diabetes Hashimoto's thyroiditis Multiple sclerosis Coeliac disease Giant cell arteritis Postorgasmic illness syndrome Reactive arthritis
GVHD	Transfusion-associated graft-versus-host disease

Unknown/
multiple

Foreign	Hypersensitivity pneumonitis Allergic bronchopulmonary aspergillosis Transplant rejection Latex allergy (I+IV)
Autoimmune	Sjögren syndrome Autoimmune hepatitis Autoimmune polyendocrine syndrome APS1 APS2 Autoimmune adrenalitis Systemic autoimmune disease

This page was last edited on 15 March 2024, at 13:07

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