Hypersensitivity reactions (HSR) are immunologic responses to an antigen that are damaging to the host. They can be divided into four distinct categories numbered (with Roman numerals) I to IV. They are distinguished by their mechanism and the cells involved. Type I reactions are allergies; type II-IV are autoimmune diseases.[1]

Type I HSRs are allergies and their antigens are frequently said to be allergens. They are characterized by IgE production (which is part of the sensitization process to the antigen), this IgE becomes bound to mast cells and upon repeat contact with the offending antigen triggers mast cell activation, leading to the release of histamine and other mediators, which causes hypotension, oedema, skin reactions (e.g., hives), asthma, etcType II HSRs are antibody-mediated reactions (specifically IgG, IgM-mediated), they can be due antibody-directed cell-mediated toxicity or due to antibodies interfering with normal cellular signalling via binding to receptors not meant for them (e.g., in myasthenia gravis the antibodies bind to nicotinic acetylcholine receptors). Type III HSRs are immune complex-mediated reactions and are due to the deposition of the immune complex in the tissues, especially the blood vessels (leading to vasculitis), joints and kidneys (causing glomerulonephritis). Type IV HSRs are cell-mediated reactions mediated by CD4+/CD8+ T-cells.[1]

Type I hypersensitivity reactionsEdit

Type HSR without title

Figure 1: Diagram showing the major events involved in type I hypersensitivity reactions

These occur after sensitization to an antigen (called an allergen in this context), which stimulates naive helper T-cells to differentiate into TH2 cells, which in turn stimulate B cells to isotype switch from IgM to IgE antibodies (usually via releasing interleukin-4 and interleukin-13). The TH2 cells also release interleukin-5 which stimulates the recruitment of eosinophils, which play a role in the delayed part of the reaction. IgE antibodies bind to FcεRI receptors on mast cells, then when these mast cells come into contact with the antigen again they activate releasing several chemical mediators such as histamine (which plays a crucial role in the immediate phase of the reaction), leukotrienes, prostaglandin D2, etc.[1]

FcεRI-α as depicted by 2Y7Q

Figure 2: Alpha subunit of FcεRI

Examples of type I hypersensitivities
Reaction ICD-10 Target tissue(s)
Allergic rhinitis (hay fever) J30 Nasal passages, eyes
Anaphylaxis T78.2 Systemic.
Angioedema D84.1, T78.3 Skin, mucus membranes.
Asthma J45 Airways.
Atopic dermatitis L20 Skin.
Urticaria (hives) L50 Skin.

Type II hypersensitivity reactionsEdit

Type II hypersensitivity reactions (T2HRs) are autoimmune diseases associated with the direct consequences of antibodies reacting against autoantigens. These antibodies are of the isotypes IgG or IgM; consequently T2HRs are due to at least one of the following four antibody-dependent mechanisms of cell damage or signalling disruption: antibody-dependent cell-mediated cytotoxicity (ADCC which is due to IgG), complement-dependent cytotoxicity (CDC; due to IgG/IgM), opsonization and phagocytosis and cellular dysfunction via interfering with the binding of ligand (e.g., acetylcholine for myasthenia gravis) to their respective receptors (nicotinic acetylcholine receptors in the neuromuscular junction for myasthenia gravis).[1]

External linksEdit

Reference listEdit

  1. 1.0 1.1 1.2 1.3 Kumar, V; Abbas, AK; Aster, AC (July 2014). "Chapter 6. Diseases of the Immune System". Robbins & Cotran Pathologic Basis of Disease 9e. Philadelphia, USA: Saunders. ISBN 978-0-8089-2450-0. 

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