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Review
. 2018 Jul 9;23(7):1665.
doi: 10.3390/molecules23071665.

Interleukin-33: Its Emerging Role in Allergic Diseases

Wen Ding  1 , Gui-Lin Zou  2 , Wei Zhang  3 , Xing-Ning Lai  4 , Hou-Wen Chen  5 , Li-Xia Xiong  6
Affiliations
Review

Interleukin-33: Its Emerging Role in Allergic Diseases

Wen Ding et al. Molecules. .

Abstract

Allergic diseases, which include asthma, allergic rhinitis (AR), chronic rhinosinusitis (CRS), atopic dermatitis (AD), food allergy (FA), allergic keratoconjunctivitis, seriously affect the quality of life of people all over the world. Recently, interleukin-33 (IL-33) has been found to play an important role in these refractory disorders, mainly by inducing T helper (Th) 2 immune responses. This article reviews the mobilization and biological function of IL-33 in allergic disorders, providing novel insights for addressing these hypersensitive conditions.

Keywords: Th2-type immunity; allergic diseases; asthma; interleukin-33; target therapy.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
IL-33 signaling pathway. IL-33 binds with ST2 transmembrane isoform and IL-1 receptor accessory protein (IL-1RAcP), leading to the downstream activation of several signaling pathways. MyD88 recruitment at TIR domain is essential for IL-33-ST2-mediated signaling cascade. On one hand, the downstream activation of TRAF6 and IRAK4 proteins activates the inhibitor of nuclear factor-κB kinase (IKK) complex, leading to NF-κB activation. On the other hand, in the absence of TRAF6, downstream activation of MAPKs leading to activation of AP-1. Next, NF-κB and AP-1 bind to DNA and induce the expression of various Th2-related cytokines, chemokines and antibodies. sST2 acts as a decoy receptor and results in the competitive inhibition of IL-33 biological activity. Single Ig IL-1R-related molecule (SIGIRR) acts as negative regulator for TIR signaling, leading to the suppression of IL-33/ST2 signaling pathways.
Figure 2
Figure 2
IL-33 in asthma pathology. IL-33 is involved in the initiation and perpetuation of airway hyperresponsiveness (AHR), airway remodeling and inflammation in asthma process.
See this image and copyright information in PMC

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