Low IL-13Rα1 expression on mast cells tunes them unresponsive to IL-13.

Autor:	Salomaa T; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.; Fimlab Laboratories, 33520 Tampere, Finland.; Northern Finland Laboratory Centre (NordLab), 90220 Oulu, Finland., Kummola L; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland., González-Rodríguez MI; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.; Fimlab Laboratories, 33520 Tampere, Finland.; Northern Finland Laboratory Centre (NordLab), 90220 Oulu, Finland., Hiihtola L; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.; Fimlab Laboratories, 33520 Tampere, Finland., Järvinen TAH; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.; Department of Orthopaedics and Traumatology, Tampere University Hospital, 33520 Tampere, Finland., Junttila IS; Faculty of Medicine and Health Technology, Tampere University, 33014 Tampere, Finland.; Fimlab Laboratories, 33520 Tampere, Finland.; Northern Finland Laboratory Centre (NordLab), 90220 Oulu, Finland.; Research Unit of Biomedicine, University of Oulu, 90570 Oulu, Finland.
Jazyk:	angličtina
Zdroj:	Journal of leukocyte biology [J Leukoc Biol] 2023 Jul 27; Vol. 114 (2), pp. 187-194.
DOI:	10.1093/jleuko/qiad065
Abstrakt:	Cytokine-mediated mast cell regulation enables precise optimization of their own proinflammatory cytokine production. During allergic inflammation, interleukin (IL)-4 regulates mast cell functions, tissue homing, and proliferation, but the direct role of closely related IL-13 for mast cell activation remains unclear. Previous work has shown that mast cells are potent IL-13 producers, but here we show that mouse mast cells do not directly respond to IL-13 by Stat6 activation, as they do not express measurable amount of IL-13 receptor α1 (IL-4Rα1) messenger RNA. Consequently, IL-4 responses are mediated via type I IL-4R (IL-4/IL4Rα/γC), and IL-4-induced Stat6 activation is abolished in γC-deficient mast cells. Type II IL-4R deficiency (IL-13Rα1 knockout) has no effect on IL-4-induced Stat6 activation. In basophils, both IL-4 and IL-13 induce Stat6 activation in wild-type and γC-deficient cells, while in type II IL-4R-deficient basophils, IL-4 signaling is impaired at low ligand concentration. Thus, mast cell and basophil sensitivity to IL-4/IL-13 is different, and in mast cells, lack of IL-13Rα1 expression likely explains their unresponsiveness to IL-13. Competing Interests: Conflict of interest statement. None declared. (© The Author(s) 2023. Published by Oxford University Press on behalf of Society for Leukocyte Biology.)
Databáze:	MEDLINE
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