Immunopathological reaction type I

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Clinical picture of atopic eczema

Immunopathological reaction of type I (anaphylactic, atopic type) is a humoral reaction, based on antibodies of the IgE class. The most common type of allergy is associated with the formation of IgE against some exoantigens:

  • penicillin causes allergies - the reactive cyclic lactam group reacts with the amino acids of various serum and cellular proteins and covalently modifies them. Antibodies, including IgE, are formed in some individuals against these newly formed epitopes and an atopic reaction occurs.
  • components of pollen grains,
  • antigens of dust mites,
  • food antigens,
  • animal fur, saliva and epithelium.

It is also the only immunopathological reaction that does not occur in autoimmune diseases. Individuals with a predisposition to react to harmless antigens by producing IgE are called atopics. That is why this type of hypersensitivity is sometimes called atopy.

Some forms of atopy correlate with certain types of MHC polymorphism, IL-4, subunits β high-affinity IgE receptor (FceR-I). The influence of the environment is also important:

  • rate of allergen exposure
  • climate factors
  • diets in infancy (breast milk and its substitutes),
  • infection: repeated respiratory viral infections lead to bronchial hyperreactivity,
  • the absence of "intestinal parasites" in developed countries during childhood leads to susceptibility to IgE reaction against harmless antigens.

According to the speed of onset, we divide this type of allergy into "early" and "late" hypersensitivity.

Early-type hypersensitivity[edit | edit source]

The reaction occurs very quickly after contact with the allergen (minutes). At the first encounter with the antigen, the patient is 'sensitization. This reaction is similar to those with which the immune system physiologically responds to multicellular parasites. Differentiation of specific clones of TH2-lymphocytes is stimulated, followed by B-lymphocytes. They secrete antibodies of the type IgE under the influence of cytokines (IL-4, IL-5). IgE antibodies bind to high-affinity IgE-receptors of mast cells and basophils. After a repeated encounter with an allergen, IgE molecules are bridged, receptors aggregate on the surface of these cells and their granules are immediately released (phase 1 of the allergic reaction):

This is followed by synthesis of signals and release of metabolites, such as arachidonic acid (phase 2 of the allergic reaction).

Progress[edit | edit source]

An allergic reaction takes place depending on the input of the allergen:

Searchtool right.svg For more information see Anaphylactic Shock.

Treatment[edit | edit source]

  • Prophylaxis: avoiding the allergen.
  • Use of pharmaceuticals blocking histamine receptors (antihistamines), inhibiting histamine synthesis, anti-inflammatory (corticoids), inhibiting degranulation (cromoglycate).
  • Hyposensitization: partially successful, gradually increasing doses of the allergen are administered, with appropriate application a partial shift from the TH2 to TH1 lymphocyte subset can be achieved, which inhibits the production of allergenic IgE.

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External links[edit | edit source]

References[edit | edit source]

  • HOŘEJŠÍ, Václav – BARTŮŇKOVÁ, Jiřina. Základy imunologie. 3. edition. Praha : Triton, 2008. 280 pp. ISBN 80-7254-686-4.