Authors:	Klebow, Sabrina Hahn, Matthias Nikoalev, Alexei Wunderlich, F. Thomas Hövelmeyer, Nadine Karbach, Susanne Waisman, Ari
Title:	IL-6 signaling in myelomonocytic cells is not crucial for the development of IMQ-induced psoriasis
Online publication date:	4-Oct-2022
Year of first publication:	2016
Language:	english
Abstract:	Psoriasis is an autoimmune skin disease that is associated with aberrant activity of immune cells and keratinocytes. In mice, topical application of TLR7/8 agonist IMQ leads to a skin disorder resembling human psoriasis. Recently, it was shown that the IL-23/ IL-17 axis plays a deciding role in the pathogenesis of human psoriasis, as well as in the mouse model of IMQ-induced psoriasis-like skin disease. A consequence of IL-17A production in the skin includes increased expression and production of IL-6, resulting in the recruitment of neutrophils and other myelomonocytic cells to the site of inflammation. To further investigate and characterize the exact role of IL-6 signaling in myelomonocytic cells during experimental psoriasis, we generated mice lacking the IL-6 receptor alpha specifically in myelomonocytic cells (IL-6RαΔmyel). Surprisingly, disease susceptibility of these mice was not affected in this model. Our study shows that classical IL-6 signaling in myelomonocytic cells does not play an essential role for disease development of IMQ-induced psoriasis-like skin disease.
DDC:	610 Medizin 610 Medical sciences
Institution:	Johannes Gutenberg-Universität Mainz
Department:	FB 04 Medizin
Place:	Mainz
ROR:	https://ror.org/023b0x485
DOI:	http://doi.org/10.25358/openscience-7806
Version:	Published version
Publication type:	Zeitschriftenaufsatz
License:	CC BY
Information on rights of use:	https://creativecommons.org/licenses/by/4.0/
Journal:	PLoS one 11 3
Pages or article number:	e0151913
Publisher:	PLoS
Publisher place:	Lawrence, Kan.
Issue date:	2016
ISSN:	1932-6203
Publisher URL:	http://dx.doi.org/10.1371/journal.pone.0151913
Publisher DOI:	10.1371/journal.pone.0151913
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)