Interleukin-3 stabilizes CD124/IL-4α surface expression in mast cells via Tyk2 and STAT6.

Autor: Drube S; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany., Strotmann B; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany., Wegner P; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany., Jäger UM; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany., Küchler C; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany., Andreas N; Institute of Immunology, Universitätsklinikum Jena, Friedrich-Schiller-Universität Jena, Jena, Germany.
Jazyk: angličtina
Zdroj: Immunology [Immunology] 2023 May; Vol. 169 (1), pp. 102-112. Date of Electronic Publication: 2022 Dec 19.
DOI: 10.1111/imm.13614
Abstrakt: Interleukin (IL)-4 signals can modulate mast cells, which express the IL-4Rα chain. The IL-4Rα can heterodimerise with the common γ-chain and utilizes JAK1 and JAK2 for signal transduction, while complexes of IL-4Rα with IL-13Rα1 subunit mediates signals via JAK2 and Tyk2. Here, we report that IL-3 is an essential factor for the continuous expression of the IL-4Rα chain on mast cells, which did not express the IL-13Rα1 chain. We demonstrate that the signals induced by IL-3 important for IL-4Rα expression are mediated by Tyk2 and STAT6 activation and the subsequent maintenance of HSP90 levels. In line with that, inhibition of either Tyk2, STAT6 or HSP90 impaired the IL-3-induced IL-4Rα upregulation. Consequently, the IL-3 maintained IL-4Rα surface expression via Tyk2 is essential for the costimulatory effect of IL-4 on the IL-33-induced production of IL-6 and IL-13.
(© 2022 The Authors. Immunology published by John Wiley & Sons Ltd.)
Databáze: MEDLINE
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