Abstract
Type 1 allergies, involve a complex interaction between dendritic cells and other immune cells, are pathological type 2 inflammatory immune responses against harmless allergens. Activated dendritic cells undergo extensive phenotypic and functional changes to exert their functions. The activation, differentiation, proliferation, migration, and mounting of effector reactions require metabolic reprogramming. Dendritic cells are important upstream mediators of allergic responses and are therefore an important effector of allergies. Hence, a better understanding of the underlying metabolic mechanisms of functional changes that promote allergic responses of dendritic cells could improve the prevention and treatment of allergies. Metabolic changes related to dendritic cell activation have been extensively studied. This review briefly outlines the basis of fatty acid oxidation and its association with dendritic cell immune responses. The relationship between immune metabolism and effector function of dendritic cells related to allergic diseases can better explain the induction and maintenance of allergic responses. Further investigations are warranted to improve our understanding of disease pathology and enable new treatment strategies.
Highlights
Allergic diseases are an increasing health challenge worldwide
The main effector cells involved in the establishment and initiation of allergic responses are antigen-presenting cells (dendritic cells (DCs) and macrophages), T helper 2 (Th2) cells, plasma cells producing IgE, eosinophils, basophils, mast cells, and innate lymphocyte type 2 cells (ILC2s)
Reported that pollen-derived E1-phytoprostanes modulate DC function via peroxisome proliferator-activated receptor (PPAR)-γ-dependent pathways which inhibits NF-κB activation thereby reducing IL-12 production by DCs and consecutive Th2 polarization [70]. Consistent with these findings, Hammad et al showed that the activation of PPAR-γ in DCs inhibits the development of eosinophilic airway inflammation in a mouse model of asthma
Summary
Allergic diseases are an increasing health challenge worldwide. In developed countries, IgE-mediated type 1 hypersensitivity disorders have been reported to affect more than 25% of the population [1]. DCs, key mediators of the immune response [2], are the most powerful professional antigen-presenting cells in the body and can efficiently ingest, process, and present antigens. They are the only antigen-presenting cells that can activate nonsensitized naive T cells and are central to the initiation, regulation, and maintenance of the immune response. FAO reprogramming plays an important role in maintaining and establishing the phenotype and function of immune cells, which include DCs [9], macrophages [10], CD4+ T [11], and ILC2s [12]. This review briefly introduces the fundamental principle of cellular FAO and its relationship with DC function and discusses the metabolic adaptation associated with the activation of DCs in the context of allergies
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