Allergy (overview) A1.0

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Allergy; Allergy of the immediate type; Cytotoxic reaction; Immediate type reaction; Instant Type Allergy; late-type allergy; Late type allergy; Late type reaction; Pathogenic immune reactions; Type I allergy; type II allergy; Type III allergy; Type IV allergy; Type V allergy; Type VI allergy

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Allergies manifest themselves in numerous organs, whereby skin and mucous membranes are particularly frequently affected (interfaces where the individual organism comes into contact with the surrounding tissue. A general classification can be made as follows:

  • Organs (allergy of the skin, lungs, nose, eye)
  • Pathomechanisms (classification according to the classification scheme of Cooms and Gell)
  • All sources (food allergy, animal hair allergy; insect venom allergy
  • Molecular allergens (e.g. Bet V 1, Ara h1 etc.)
  • Course and prognosis (acute or chronic allergy)
  • Genetic aspects (e.g. hereditary allergy, sporadic allergy)
  • Age (childhood allergy, allergies in old age)

Classification according to pathomechanisms (Coombs and Gell 1963): According to the (classical) classification of Coombs and Gell, 4 or 6 immunological reaction types of hypersensitivity can be distinguished (for didactic reasons), although this classification is difficult in the clinic due to overlapping reaction sequences.

Type I reaction (hypersensitivity of the immediate type): In this case antigen contact (allergen contact e.g. of a drug) by cross-linking of juxtaposed, membrane-bound IgE antibodies on mast cells and basophilic granulocytes for cell activation and release of preformed mediators ( histamine, heparin, tryptase, ECP = eosinophilic cationic protein) and newly generated mediators such as leukotrienes (LTC4, LTD4, LTB4), prostaglandins, thrombboxanes and platelet-aggregating factor ( PAF). Typical diseases of type I allergy:

Type II reaction (humoral cytotoxic reaction): After binding of antibodies (IgG, IgM) to cellular antigens, lysis of the target cell occurs by activation of the complement cascade and by the action of cytotoxic cells (killer cells, platelets, eosinophil and neutrophil granulocytes, monocytes/macrophages). While the sensitization phase with the formation of corresponding antibodies takes about 5-10 days, the effector phase lasts about 2-3 days until clinical symptoms appear. Typical diseases with an underlying type II allergy:

  • allergic haemolytic anaemia

  • Thrombopenia (thrombocytopenic purpura)

  • Agranulocytosis

  • Transfusion incidents

  • Goodpasture's Syndrome

Type III reaction

  • Immunocomplex reaction: Triggers are aggregates of allergen (often drug) haptens + carrier protein and the antibodies or complexes induced thereby, which are composed exclusively of allergen-specific immunoglobulins. These can precipitate in the postcapillary venules and cause leukocytoclastic vasculitis. The sensitization phase lasts about 10 days, the effector phase until the clinical symptoms appear 2-5 days.

  • Serum Disease: Here an immune complex reaction proceeds rapidly due to an excessive activation of the complement system. For example, after two parenteral administrations of foreign protein components, the formation and deposition of circulating immune complexes leads to massive and acute complement activation and leukocytoclasia.

  • Immunocomplex disease in autoimmunity: e.g. chronic polyarthritis (rheumatoid arthritis); lupus erythematosus, systemic; vasculitis, leukocytoclastic; polyarteritis; fibrosing alveolitis.

  • Immunocomplex disease associated with sensitization to environmental antigens: e.g. exogenous allergic alveolitis (avian lung, farmer's lung, byssinosis, cotton fever).

Type IV reaction (cell-mediated reaction, hypersensitivity of the delayed type). Effector cells are allergen-specific inflammatory and cytotoxic T cells.

  • Type IV reaction: Type IV allergy is the most common form of allergy after type I allergy. Local inflammatory reaction within 24 hours by infiltration of the epidermis with basophilic granulocytes. The clinical prototype of the type IV reaction is the allergic contact eczema. The reaction to allergen contact, in which the allergen (contact allergen) penetrates the epidermis, begins within 48-72 hours. Contact with specific T-cells leads to alteration of the epidermis through release of lymphokines. Depending on the lymphocyte population significantly involved, an immunological subdivision of the reactions into classes IVa-IVd has been proposed (Pfützner W 2018).

    • Type IVa: INF-gamma and/or TNF-alpha secreting CD4+ T-helper cells (Th1-type)

    • Type IVb: IL-5 (and IL-4, IL-13) secreting CD4+-T-helper cells (Th2-type) are mainly responsible for the mobilization and activation of eosinophilic granulocytes.

    • Type IVc: Perforin- and granzyme-B-producing CD8+ cytotoxic T cells are the essential effector cells of many drug reactions. Depending on the extent of T-cell activation and the release of perforin and granzyme B, reversible keratinocyte damage of varying degrees (dyskeratosis cell necrosis) occurs

    • Type IVd: Indicators are CXCL8 and GM-CSF producing T cells (CXCL8 stands for CXC motif chemokine 8). They are mainly responsible for the recruitment of neutrophilic granulocytes. This mechanism plays a role in acute generalized exanthematic pustulose (AGEP).

Type V (granulomatous reaction): 12 hours after injection of tuberculin, the infiltration of T-lymphocytes in a sensitized organism leads to a local perivascular inflammatory reaction. The release of lymphokines and cytotoxic factors causes tissue damage. The persistence of pathogens or other exogenous material results in a granulomatous inflammation, usually interspersed with giant cells.

Type VI (immunodeviation): Mainly biologicals such as TNF-alpha antagonists or different types of immunodeficiency drugs. Immune checkpoint inhibitors can trigger inflammatory or autoimmunological reactions by stimulating inflammatory T cell populations, inducing autoantibodies or suppressing regulatory T cells(Treg). An example is the triggering of autoimmune phenomena in melanoma patients treated with CTLA-4 or PD1 antibodies. Furthermore, autoimmune thyroiditis, myasthenia gravis, forms of insulin resistance, etc. are assigned to this type of allergic reaction

A classification proposed by Johansson et al. divides hypersensitivity for clinical reasons into immunological and non-immunological (pseuoallergies).

Clinical features
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Type I reaction: Within seconds to minutes conjunctivitis, rhinitis, bronchial asthma, shock, anaphylactic, urticaria, angioedema (see also pollinosis), diarrhea, vomiting. Aeroallergens (e.g. pollen) play an important role in the Type I reaction. These allergens can be absorbed not only through the mucous membrane (by inhalation) but also percutaneously through the skin. This mechanism plays a role in the seasonal exacerbation of atopic dermatitis (especially in exposed skin areas). Remarkably, type I sensitizations in children are associated with an increased CRP value (Chawes et al. 2017).

Type II reaction: onset within hours. Haemolytic anaemia (e.g. haemolyticus neonatorum disease, transfusion incident), allergic thrombopenia, allergic granulopenia, Goodpasture's syndrome, myasthenia gravis, autoimmune thyroiditis, pemphigus and pemphigoid.

Type III reaction:

  • Arthus reaction: onset within 12 hours of injection. More or less haemorrhagic oedema develops at the injection site and subsides significantly within 48-72 hours, e.g. local vaccination reaction after overvaccination with tetanus antigen.
  • Serum disease: onset within a few hours with nephritis, arthritis, urticarial or extensive redness.
  • Infectallergic immune complex disease, e.g. leprosy, malaria, bacterial endocarditis, leukocytoclastic vasculitis, hepatitis.

Type IV reaction (late type reaction):

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Besides causal therapy, allergy prevention also plays a decisive role in treatment.

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Last updated on: 29.10.2020