The impact of type 2 immunity and allergic diseases in atherosclerosis

免疫学 医学 过敏 免疫 免疫系统
作者
Nieves Fernández‐Gallego,Raquel Castillo‐González,Nerea Méndez‐Barbero,Celia López‐Sanz,David Obeso,Alma Villaseñor,María M. Escribese,Beatriz López‐Melgar,Jorge Salamanca,Amparo Benedicto‐Buendía,Luis Jesús Jiménez‐Borreguero,Borja Ibáñez,J. Sastre,María Teresa Belver,Francisco Vega,Carlos Blanco,Domingo Barber,Francisco Sánchez‐Madrid,Hortensia de la Fuente,Pilar Martı́n,Vanesa Esteban,Rodrigo Jiménez‐Saiz
出处
期刊:Allergy [Wiley]
卷期号:77 (11): 3249-3266 被引量:36
标识
DOI:10.1111/all.15426
摘要

Abstract Allergic diseases are allergen‐induced immunological disorders characterized by the development of type 2 immunity and IgE responses. The prevalence of allergic diseases has been on the rise alike cardiovascular disease (CVD), which affects arteries of different organs such as the heart, the kidney and the brain. The underlying cause of CVD is often atherosclerosis, a disease distinguished by endothelial dysfunction, fibrofatty material accumulation in the intima of the artery wall, smooth muscle cell proliferation, and Th1 inflammation. The opposed T‐cell identity of allergy and atherosclerosis implies an atheroprotective role for Th2 cells by counteracting Th1 responses. Yet, the clinical association between allergic disease and CVD argues against it. Within, we review different phases of allergic pathology, basic immunological mechanisms of atherosclerosis and the clinical association between allergic diseases (particularly asthma, atopic dermatitis, allergic rhinitis and food allergy) and CVD. Then, we discuss putative atherogenic mechanisms of type 2 immunity and allergic inflammation including acute allergic reactions (IgE, IgG1, mast cells, macrophages and allergic mediators such as vasoactive components, growth factors and those derived from the complement, contact and coagulation systems) and late phase inflammation (Th2 cells, eosinophils, type 2 innate‐like lymphoid cells, alarmins, IL‐4, IL‐5, IL‐9, IL‐13 and IL‐17).
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