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Type I hypersensitivity

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]

Type I hypersensitivity
Other namesImmediate hypersensitivity
Image showing the mechanism of activation of type 1 hypersensitivity in a mast cell.
SpecialtyImmunology

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

Pathophysiology edit

In type I hypersensitivity, B cells are stimulated (by CD4+ Th2 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.

 
A summary of the pathophysiology of a type 1 hypersensitivity reaction.

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
Smooth muscle spasm
  • Histamine
  • PAF
  • Leukotriene C4, D4, and E4
  • Prostaglandin
Leukocyte extravasation
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 edit

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 edit

Some examples:

See also edit

References edit

  1. ^ med/1101 at eMedicine
  2. ^ 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.
  3. ^ . Archived from the original on 2010-07-27. Retrieved 2008-09-22.
  4. ^ 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
  5. ^ Abbas, M., Moussa, M., & Akel, H. (2021, July 21). Type I hypersensitivity reaction. StatPearls [Internet]. Retrieved November 29, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK560561/.
  6. ^ 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.
  7. ^ 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…”
  8. ^ Recognizing and Treating Reaction Symptoms. (n.d.). Retrieved December 01, 2020, from https://www.foodallergy.org/resources/recognizing-and-treating-reaction-symptoms. “Although steroids do not work fast enough for emergency treatment, they may help prevent a severe reaction from coming back…antihistamines are prescribed to relieve mild allergy symptoms.”

External links edit

type, hypersensitivity, immediate, hypersensitivity, gell, coombs, classification, allergic, reactions, allergic, reaction, provoked, exposure, specific, type, antigen, referred, allergen, type, distinct, from, type, type, type, hypersensitivities, relevance, . 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 Type I hypersensitivityOther namesImmediate hypersensitivityImage showing the mechanism of activation of type 1 hypersensitivity in a mast cell SpecialtyImmunologyExposure may be by ingestion inhalation injection or direct contact Contents 1 Pathophysiology 2 Treatment and prognosis 3 Examples 4 See also 5 References 6 External linksPathophysiology editIn type I hypersensitivity B cells are stimulated by CD4 Th2 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 FceRI 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 nbsp A summary of the pathophysiology of a type 1 hypersensitivity reaction 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 proteasesSmooth muscle spasm Histamine PAF Leukotriene C4 D4 and E4 ProstaglandinLeukocyte extravasation Cytokines e g chemokines and TNF Leukotriene B4 Chemotactic factors for neutrophils and eosinophilsUnless 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 editIf 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 editSome examples Allergic asthma Allergic conjunctivitis Allergic rhinitis hay fever Anaphylaxis Angioedema Urticaria hives Eosinophilia Penicillin allergy Cephalosporin allergy Food allergy Sweet itchSee also editHypersensitivityReferences edit med 1101 at eMedicine Descotes Jacques Choquet Kastylevsky Genevieve 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 FceRI crosslinking Figure 1 Mediator release from mast cellsFigure 2 Model of genesis of mast cell secretory granulesFigure 3 Lipid body biogenesisTable 2 Stimuli selective mediator release from mast cells Abbas M Moussa M amp Akel H 2021 July 21 Type I hypersensitivity reaction StatPearls Internet Retrieved November 29 2021 from https www ncbi nlm nih gov books NBK560561 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 amp 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 b adrenergic properties of epinephrine cause bronchodilation Epinephrine administration enhances coronary blood flow Recognizing and Treating Reaction Symptoms n d Retrieved December 01 2020 from https www foodallergy org resources recognizing and treating reaction symptoms Although steroids do not work fast enough for emergency treatment they may help prevent a severe reaction from coming back antihistamines are prescribed to relieve mild allergy symptoms External links edit Retrieved from https en wikipedia org w index php title Type I hypersensitivity amp oldid 1185600986, wikipedia, wiki, book, books, library,

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