Allergic Rhinitis (AR) is an IgE-mediated hypersensitivity disease caused by inhalation of an allergen to which the patients is sensitized. Etiopathogenesis of AR comprises a sensitization phase, an immediate phase and a late phase. In the sensitization phase, inhaled allergens are processed in peptides and come into contact with the nasal mucosa cells. Antigen-Presenting Cells (APCs), especially represented by Dendritic Cells (DCs), capture them through the interaction with their own MHC class II complexes and migrate to lymph nodes. Then, allergenic peptides are presented to naïve CD4+ T lymphocytes and a differentiation of T cells in Th2 subset takes place. After Th2 lymphocyte induction due to allergen exposure, the most relevant cytokines that are produced are represented by IL-3, IL-4, IL-5, IL-9, IL-10, and IL-13 that are able to promote IgE synthesis and mast cell proliferation. The allergen reaction, when allergen meets its specific IgEs on mast cells surface, causes an early inflammatory reaction determined by mast cells and basophils degranulation with release of preformed mediators from the intracellular granules, resulting in symptoms such as rhinorrhea, itching and sneezing. This phase is followed by a late phase characterized by the release of newly formed mediators, like leukotrienes, chemokines and adhesion molecules, and by the recruitment of eosinophils, neutrophils, macrophages, mast cells, lymphocytes B and T in the nasal mucosa. Such mechanism is responsible for continuing inflammation sustained by chemoattractants, cytokines and adhesion receptors that induce cellular infiltration of eosinophils, basophils, Th2 lymphocytes and mast cells and is clinically mirrored by the prevalence of nasal congestion over sneezing, itching and rhinorrhea.

Mechanisms of allergic diseases in Otorhinolaryngology / Ridolo, E; Martignago, I; Masieri, S. - In: JOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS. - ISSN 0393-974X. - 32:1 Suppl. 1(2018), pp. 9-12.

Mechanisms of allergic diseases in Otorhinolaryngology

Ridolo, E;Martignago, I;
2018

Abstract

Allergic Rhinitis (AR) is an IgE-mediated hypersensitivity disease caused by inhalation of an allergen to which the patients is sensitized. Etiopathogenesis of AR comprises a sensitization phase, an immediate phase and a late phase. In the sensitization phase, inhaled allergens are processed in peptides and come into contact with the nasal mucosa cells. Antigen-Presenting Cells (APCs), especially represented by Dendritic Cells (DCs), capture them through the interaction with their own MHC class II complexes and migrate to lymph nodes. Then, allergenic peptides are presented to naïve CD4+ T lymphocytes and a differentiation of T cells in Th2 subset takes place. After Th2 lymphocyte induction due to allergen exposure, the most relevant cytokines that are produced are represented by IL-3, IL-4, IL-5, IL-9, IL-10, and IL-13 that are able to promote IgE synthesis and mast cell proliferation. The allergen reaction, when allergen meets its specific IgEs on mast cells surface, causes an early inflammatory reaction determined by mast cells and basophils degranulation with release of preformed mediators from the intracellular granules, resulting in symptoms such as rhinorrhea, itching and sneezing. This phase is followed by a late phase characterized by the release of newly formed mediators, like leukotrienes, chemokines and adhesion molecules, and by the recruitment of eosinophils, neutrophils, macrophages, mast cells, lymphocytes B and T in the nasal mucosa. Such mechanism is responsible for continuing inflammation sustained by chemoattractants, cytokines and adhesion receptors that induce cellular infiltration of eosinophils, basophils, Th2 lymphocytes and mast cells and is clinically mirrored by the prevalence of nasal congestion over sneezing, itching and rhinorrhea.
Mechanisms of allergic diseases in Otorhinolaryngology / Ridolo, E; Martignago, I; Masieri, S. - In: JOURNAL OF BIOLOGICAL REGULATORS & HOMEOSTATIC AGENTS. - ISSN 0393-974X. - 32:1 Suppl. 1(2018), pp. 9-12.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11381/2842396
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