Allergy (overview) A1.0

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 23.04.2021

Dieser Artikel auf Deutsch

Synonym(s)

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

Classification
This section has been translated automatically.

Allergies manifest themselves in numerous organs, with skin and mucous membranes being particularly frequently affected (interfaces at which the individual organism comes into contact with the environment). A general classification can be made as follows according to:

  • organs (allergy of the skin, lungs, nose, eye)
  • pathomechanisms (classification according to the classification scheme of Cooms and Gell)
  • Allergen sources (food allergy, animal dander 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 topathomechanisms (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): Here, after antigen contact (allergen contact e.g. of a drug), cross-linking occurs. of a drug), cross-linking of juxtaposed, membrane-bound IgE antibodies on mast cells and basophilic granulocytes leads to 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, thromboxanes 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, the complement cascade is activated and cytotoxic cells (killer cells, platelets, eosinophilic and neutrophilic granulocytes, monocytes/macrophages) act to lyse the target cell. While the sensitization phase with the formation of corresponding antibodies lasts about 5-10 days, the effector phase until the appearance of clinical symptoms lasts about 2-3 days. Typical diseases underlying a type II allergy:

  • allergic hemolytic anemia

  • Thrombocytopenia (thrombocytopenic purpura)

  • Agranulocytosis

  • Transfusion incidents

  • Goodpasture's syndrome

Type III reaction

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

  • Serum sickness: In this case, an immune complex reaction occurs rapidly due to an excessive activation of the complement system. For example, after two parenteral administrations of foreign protein components, massive and acute complement activation and leukocytoclasia occur due to the formation and deposition of circulating immune complexes.

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

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

Type IV reaction (cell-mediated reaction, delayed-type hypersensitivity): 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 starting within 24 h by infiltration of the epidermis with basophilic granulocytes. The clinical prototype of the type IV reaction is allergic contact dermatitis. Within 48-72 hrs onset of reaction to allergen contact in which the allergen (contact allergen) penetrates the epidermis. Contact with specific T cells leads to alteration of the epidermis through the 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 mobilization and activation of eosinophil granulocytes.

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

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

Type V (Granulomatous reaction): 12 h after injection of tuberculin, local perivascular inflammatory reaction occurs in a sensitized organism due to infiltration of T lymphocytes. Tissue damage results from the release of lymphokines and cytotoxic factors. Persistence of pathogens or other exogenous material results in granulomatous inflammation, usually interspersed with giant cells.

Type VI (immunodeviation): V.a. biologics such as TNF-alpha antagonists or various immune checkpoint inhibitors. 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 induction of autoimmune phenomena in melanoma patients treated with CTLA-4 or PD1 antibodies. Furthermore, autoimmune thyroiditis, myasthenia gravis, forms of insulin resistance and others are assigned to this type of allergic reactions.

A classification proposed by Johansson et al. divides hypersensitivity into immmunological and non-immunological(pseudoallergies) based on clinical considerations.

Clinical features
This section has been translated automatically.

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):

Note(s)
This section has been translated automatically.

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

Literature
This section has been translated automatically.

  1. Averbeck M et al.(2007) Immunological fundamentals of allergies. JDDG 11: 1015-1028
  2. Breuer K et al (2003) The impact of food allergy in patients with atopic dermatitis. dermatologist 54: 121-129
  3. Chawes BL et al (2017) Allergic sensitization at school age is a systemic low-grade inflammatory disorder. Allergy 72:1073-1080.
  4. Guideline of the German Society for Allergology and Clinical Immunology (DGAI) in cooperation with the German Dermatological Society (DDG), Action Alliance for Allergy Prevention. AWMF Guideline Register No. 061/016
  5. Ingordo V et al (2003) Adult-onset atopic dermatitis in a patch test population. Dermatology 206: 197-203
  6. Johansson SG et al (2001) A revised nomenclature for allergy. Allergy 2001 56: 813-824
  7. Jakobi U et al (2003) Penetration of pollen allergens by skin development of a new detection method. Act Dermatol 29: 202-205
  8. Johansson C et al (2003) Atopy patch test reactions to Malassezia allergens differentiate subgroups of atopic dermatitis patients. Br J Dermatol 148: 479-488
  9. Langeland T et al (1989) Studies of atopic patch tests. Acta Derm Venereol 144: 105-109
  10. Latcham F et al (2003) A consistent pattern of minor immunodeficiency and subtle enteropathy in children with multiple food allergy. J Pediatr 143: 39-47
  11. Leung DY et al (2003) Effect of anti-IgE therapy in patients with peanut allergy. N Engl J Med 348: 986-993
  12. Magnusson J et al (2003) Seasonal intestinal inflammation in patients with birch pollen allergy. J Allergy Clin Immunol 112: 45-50
  13. Metzger H (2003) Two approaches to peanut allergy. N Engl J Med 348: 1046-1048
  14. Nja F et al (2003) Airway infections in infancy and the presence of allergy and asthma in school age children. Arch Dis Child 88: 566-569
  15. Pfützner W (2018) Cutaneous drug reactions. In: Plewig G et al. (ed.) Braun-Falco`s Dermatology,Venerology and Allergology. Springer publishing house SS 559-624
  16. Safe SH (2002) Food allergy. Lancet 360: 701-710
  17. Worm M et al (2016) Guideline on the management of IgE-mediated food allergies. Allergology 39: 302-344
  18. Yuill GM et al (2003) A national survey of the provision for patients with latex allergy. Anaesthesia 58: 775-777

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

Authors

Last updated on: 23.04.2021