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. 2023 Mar 31;55(1):1156–1170. doi: 10.1080/07853890.2023.2188487

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© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 1. — IL-4 and IL-13 receptor structure IL-4 can bind to both type I and type II receptors. (A) Type I receptors consist of IL-4Rα and γc, whereas type II receptors consist of IL-4Rα and IL-13Rα1. When IL-4 binds to a type I receptor, Janus kinase (JAK) 1 and JAK3 are activated; both can induce tyrosine phosphorylation of the type I receptor intracellular domain, forming docking sites for downstream signaling molecules, such as signal transducer and activator of transcription (STAT) 6 and insulin receptor substrate-2 (IRS-2). Homodimers of STAT6 then translocate to the nucleus to facilitate transcription of IL-4- and IL-13-dependent genes. IRS-2 can activate signaling molecules, such as PI3K to induce gene transcription. (B) IL-13 binds to IL-13Rα2 with greater affinity than IL-13Rα1; the IL-13Rα2 receptor is considered a decoy receptor because it lacks a cytoplasmic signaling tail. However, the cytoplasmic domain of IL-13Rα2 may attenuate IL-4 signaling by inhibiting dimerization with γc or IL-13Rα1. (C) When IL-4 or IL-13 binds to a type II receptor, JAK1 and JAK2/TYK2 are activated.