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Type I hypersensitivity which can also be called anaphylactic or atopic hypersensitivity reaction is an IgE-mediated type of allergy that occurs immediately following the exposure or prior sensitization of the host’s body by the invasion of an allergen. It generally occurs when an allergen binds to the surface of an IgE molecule whose FC region or receptor is attached to a mast cell or basophil. This binding leads to the degranulation of the mast cells to release pharmacologically active substances (e.g., histamine and heparin) that cause adverse inflammatory reactions in the affected individuals. There is usually a short time observed between the exposure of a sensitized human host to an allergen and the appearance of clinical symptoms associated with anaphylactic reaction. This is why Type I hypersensitivity is generally regarded as an immediate-type hypersensitivity reaction.


Mast cells are immune system cells that are derived from the bone marrow cells during haematopoiesis. They are present in several tissues of the body (especially in connective tissues) where they bind to the FC region of IgE molecules to mediate inflammatory response as is obtainable in hypersensitivity reactions. Mast cells are cells that bind IgE. The effector molecule of Type I hypersensitivity is IgE. Mast cells contain numerous cytoplasmic granules that are shed following the cross-linking of an IgE molecule with an allergen in a human or animal host; and they have receptors for the FC region of immunoglobulin E on their cell surfaces. Type I hypersensitivity is an immediate-type allergic reaction; and this type of hypersensitivity reaction can be localized in nature. It can also be a systemic/generalized inflammatory response depending on the antigenicity of the invading allergen(s) amongst other factors.

In Type I hypersensitivity reaction, the host becomes sensitized to a given allergen following an initial introduction of the antigen into the host’s body. The host’s immune system produces numerous IgE against the invading allergen at the first exposure to the antigen; and the IgE molecules produced becomes attached through their FC region to receptors on the mast cells or basophils. The IgE so produced parades the general circulation in search of allergens to bind to. After some days or months past the first exposure, and the host becomes exposed to the same allergen the second time, the allergen cross-links the IgE molecules on the mast cells or basophils (i.e., the IgE attaches the allergen to the mast cells), and this result in the production of chemical or physiological or vasoactive mediators such as histamine, leukotrienes and prostaglandins – which causes an immediate anaphylactic reaction in the affected animal host (Figure 11). The degranulation of the mast cells or basophils during anaphylactic reaction is mainly mediated through the cross-linking of the IgE molecule(s).

Figure 1. Illustration of Type I hypersensitivity reaction. IgE is the main mediator of Type I hypersensitivity or anaphylactic reaction. The main biological function of this immunoglobulin molecule in anaphylactic reaction is to cross-link (i.e., act as a bridge) between the allergen that invaded the body and the mast cells or basophils which are known to contain cytoplasmic granules (e.g., histamine). The FC region of the IgE molecules binds specifically to the receptors on the mast cells or basophils while its Fab region or fragment binds to the allergen. This binding leads to the degranulation of the mast cells to release vasoactive substances such as histamine and prostaglandins – which ultimately provoke the clinical or subclinical conditions, associated with the Type I hypersensitivity. Photo courtesy: https://www.sciencedirect.com/topics/immunology-and-microbiology/type-i-hypersensitivity  

Diarrhea, urticaria, vomiting, eczema, body itching, asthma, hay fever, and food allergies are some examples of Type I hypersensitivity reaction. However, in severe or life-threatening anaphylactic reactions (e.g., disintegration of the vascular system), death can occur unless appropriate medical help (in the form of supportive therapy) is rendered to the affected human host. Type I hypersensitivity reaction is the commonest type of allergic reactions in humans. It is worthy of note that the physiological mediators produced in anaphylactic reactions also mediate a protective inflammatory reaction in the host. But in severe responses, these mediators could cause harsh medical conditions (i.e., anaphylactic reactions) in the host. The pharmacologically active substances released in Type I hypersensitivity reaction can also cause the vasodilation or constriction of smooth muscles in the body. This may affect the normal physiological functions of some vital muscular activities in the affected hosts especially in respiratory activities such as in asthma sufferers whose allergen entered the body through the respiratory tract by inhalation.

Allergens that provoke anaphylactic reaction can also enter the body through foods (i.e., by ingestion) and through direct inoculation or drug administration especially parenterally. Microbial spores, some foods especially nuts and proteinous foods, insect venoms, drugs (e.g., penicillin and sulphonamides), pollen grains from plants or flowers and dust particles are some examples of allergens that could provoke anaphylactic reactions in human or animal hosts. The clinical outcome or symptoms of Type I hypersensitivity reaction is usually affected by some host factors and other environmental conditions including but not limited to: (1) the amount or concentration of the administered allergen, (2) the route of administration of the allergen and (3) the number of times the host is exposed to the antigen or allergen. Type I hypersensitivity reaction could be prevented especially by avoiding contact with the allergen(s) responsible for the anaphylactic reaction. Anti-histamine drugs which block the release of histamine for example and other clinical remedy could also be applied in containing the adverse effects of anaphylactic reactions in affected human hosts. In life-threatening cases, it is also critical to ensure appropriate airflow (by use of ventilators) in the affected individual in order to maintain proper respiratory function of the affected human host.       

Further reading

William E.P (2003). Fundamental Immunology. 5th edition. Lippincott Williams and Wilkins Publishers, USA.

Stevens, Christine Dorresteyn (2010). Clinical immunology and serology. Third edition. F.A. Davis Company, Philadelphia.

Silverstein A.M (1999). The history of immunology. In Paul, WE (ed): Fundamental Immunology, 4th edition. Lippincott Williams and Wilkins, Philadelphia, USA.

Paul W.E (2014). Fundamental Immunology. Seventh edition. Lippincott Williams and Wilkins, USA.

Male D, Brostoff J, Roth D.B and Roitt I (2014). Immunology. Eight edition. Elsevier Saunders, USA.

Levinson W (2010). Review of Medical Microbiology and Immunology. Twelfth edition. The McGraw-Hill Companies, USA.

Berzofsky J.A and Berkower J.J (1999). Immunogenicity and antigen structure. In Fundamental Immunology, 4th edition., W.E. Paul, ed., Lippincott-Raven, Philadelphia. 

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