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The development of allergic inflammation

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Abstract

Allergic disorders, such as anaphylaxis, hay fever, eczema and asthma, now afflict roughly 25% of people in the developed world. In allergic subjects, persistent or repetitive exposure to allergens, which typically are intrinsically innocuous substances common in the environment, results in chronic allergic inflammation. This in turn produces long-term changes in the structure of the affected organs and substantial abnormalities in their function. It is therefore important to understand the characteristics and consequences of acute and chronic allergic inflammation, and in particular to explore how mast cells can contribute to several features of this maladaptive pattern of immunological reactivity.
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... Type I hypersensitivities develop as a result of activation of T helper type 2 cells (Th2) and their signature cytokines IL-4, IL-5 and IL-13 [19]. These cytokines are responsible for production of allergen specific IgE antibodies by B cells that bind to the IgE high affinity receptor, FcεRI, expressed on mast cells. ...
... These cytokines are responsible for production of allergen specific IgE antibodies by B cells that bind to the IgE high affinity receptor, FcεRI, expressed on mast cells. The binding of IgE to the FcεRI and crosslinking of bound IgE with allergen activates mast cells and causes the release of pro-inflammatory mediators [19][20][21]. Additionally, a line of recent evidence has shown that epithelial barriers play a major role in development of Type I hypersensitivities alongside Th2 cells [22][23][24]. ...
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... The allergic reaction of AR starts with the recognition of allergens by antigen-presenting cells, mainly dendritic cells, which drive type 2 T helper (Th2) cell polarization. Then, Th2 cells release various inflammatory cytokines, including IL-4, IL-5, and IL-13, leading to the recruitment of effector cells, such as eosinophils and mast cells [77,78]. These inflammatory factors and eotaxin have an important function in the generation and recruitment of effector cells, such as eosinophils, in the lower airways. ...
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