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19.1 Hypersensitivities  (Page 3/24)

On first exposure to an allergen in a susceptible individual, antigen-presenting cells process and present allergen epitopes with major histocompatibility complex (MHC) II to T helper cells. B cells also process and present the same allergen epitope to T H 2 cells, which release cytokines IL-4 and IL-13 to stimulate proliferation and differentiation into IgE-secreting plasma cells. The IgE molecules bind to mast cells with their Fc region, sensitizing the mast cells for activation with subsequent exposure to the allergen. With each subsequent exposure, the allergen cross-links IgE molecules on the mast cells, activating the mast cells and causing the release of preformed chemical mediators from granules ( degranulation ), as well as newly formed chemical mediators that collectively cause the signs and symptoms of type I hypersensitivity reactions.

Type I hypersensitivity reactions can be either localized or systemic. Localized type I hypersensitivity reactions include hay fever rhinitis , hives, and asthma ( [link] ). Systemic type I hypersensitivity reactions are referred to as anaphylaxis or anaphylactic shock . Although anaphylaxis shares many symptoms common with the localized type I hypersensitivity reactions, the swelling of the tongue and trachea, blockage of airways, dangerous drop in blood pressure, and development of shock can make anaphylaxis especially severe and life-threatening. In fact, death can occur within minutes of onset of signs and symptoms.

Late-phase reactions in type I hypersensitivities may develop 4–12 hours after the early phase and are mediated by eosinophil s, neutrophil s, and lymphocytes that have been recruited by chemotactic factors released from mast cells . Activation of these recruited cells leads to the release of more chemical mediators that cause tissue damage and late-phase symptoms of swelling and redness of the skin, coughing, wheezing, and nasal discharge.

Individuals who possess genes for maladaptive traits, such as intense type I hypersensitivity reactions to otherwise harmless components of the environment, would be expected to suffer reduced reproductive success. With this kind of evolutionary selective pressure, such traits would not be expected to persist in a population. This suggests that type I hypersensitivities may have an adaptive function. There is evidence that the IgE produced during type I hypersensitivity reactions is actually meant to counter helminth infections C.M. Fitzsimmons et al. “Helminth Allergens, Parasite-Specific IgE, and Its Protective Role in Human Immunity.” Frontier in Immunology 5 (2015):47. . Helminths are one of few organisms that possess proteins that are targeted by IgE. In addition, there is evidence that helminth infections at a young age reduce the likelihood of type I hypersensitivities to innocuous substances later in life. Thus it may be that allergies are an unfortunate consequence of strong selection in the mammalian lineage or earlier for a defense against parasitic worms .

Type I Hypersensitivities
Common Name Cause Signs and Symptoms
Allergy-induced asthma Inhalation of allergens Constriction of bronchi, labored breathing, coughing, chills, body aches
Anaphylaxis Systemic reaction to allergens Hives, itching, swelling of tongue and throat, nausea, vomiting, low blood pressure, shock
Hay fever Inhalation of mold or pollen Runny nose, watery eyes, sneezing
Hives (urticaria) Food or drug allergens, insect stings Raised, bumpy skin rash with itching; bumps may converge into large raised areas
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OpenStax, Microbiology. OpenStax CNX. Nov 01, 2016 Download for free at http://cnx.org/content/col12087/1.4
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