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Review
. 2018 Sep 4:9:2006.
doi: 10.3389/fimmu.2018.02006. eCollection 2018.

Eicosanoid Control Over Antigen Presenting Cells in Asthma

Nincy Debeuf  1   2 , Bart N Lambrecht  1   2   3
Affiliations
Review

Eicosanoid Control Over Antigen Presenting Cells in Asthma

Nincy Debeuf et al. Front Immunol. .

Abstract

Asthma is a common lung disease affecting 300 million people worldwide. Allergic asthma is recognized as a prototypical Th2 disorder, orchestrated by an aberrant adaptive CD4+ T helper (Th2/Th17) cell immune response against airborne allergens, that leads to eosinophilic inflammation, reversible bronchoconstriction, and mucus overproduction. Other forms of asthma are controlled by an eosinophil-rich innate ILC2 response driven by epithelial damage, whereas in some patients with more neutrophilia, the disease is driven by Th17 cells. Dendritic cells (DCs) and macrophages are crucial regulators of type 2 immunity in asthma. Numerous lipid mediators including the eicosanoids prostaglandins and leukotrienes influence key functions of these cells, leading to either pro- or anti-inflammatory effects on disease outcome. In this review, we will discuss how eicosanoids affect the functions of DCs and macrophages in the asthmatic lung and how this leads to aberrant T cell differentiation that causes disease.

Keywords: asthma; dendritic cells; eicosanoids; leukotrienes; macrophages; prostaglandins.

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Figures

Figure 1
Figure 1
Schematic overview of eicosanoid biosynthesis. Arachidonic acid that is released from membrane phospholipids by cytosolic phospholipase A2 (PLA2), can be enzymatically converted either to prostaglandins (PG) and thromboxane (TXA2) by COX enzymes or to LT and lipoxins (LXA4) by lipoxygenases (LOXs).
Figure 2
Figure 2
Eicosanoids have multiple effects in allergic asthma. In response to allergens and/or instructive cytokines by epithelial cells and innate immune cells, dendritic cells activate Th2 immunity in the draining lymph nodes, leading to IgE responses and to Th2 effector cells that control eosinophilic airway inflammation, goblet cell metaplasia and bronchial hyperreactivity upon return to the lung. Virtually all cell types relevant to Th2 pathology such as Th2 cells, ILC2s, mast cells, basophils and epithelial cells, generate leukotriene/prostaglandin mediators, and/or express receptors for those eicosanoids. The figure represents a schematic overview of eicosanoid functions described in this review.
See this image and copyright information in PMC

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