title: IL-6 Signaling in Myelomonocytic Cells Is Not Crucial for the Development of IMQ-Induced Psoriasis.
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.
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Sabrina
authors.initials: S
authors.lastname: Klebow
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Hahn
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Alexei
authors.initials: A
authors.lastname: Nikoalev
authors.affiliation: Max Planck Institute for Metabolism Research, Cologne, Germany.
authors.forename: F Thomas
authors.initials: FT
authors.lastname: Wunderlich
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Nadine
authors.initials: N
authors.lastname: Hövelmeyer
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.|Department of Medicine 2, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Susanne H
authors.initials: SH
authors.lastname: Karbach
authors.affiliation: Institute for Molecular Medicine, University Medical Center of the Johannes-Gutenberg University of Mainz, Mainz, Germany.
authors.forename: Ari
authors.initials: A
authors.lastname: Waisman
mesh_terms: D000634:Aminoquinolines / Q000009:adverse effects*; D000818:Animals; D001853:Bone Marrow / Q000473:pathology; D002451:Cell Compartmentation; D017353:Gene Deletion; D006801:Humans; D000077271:Imiquimod; D015850:Interleukin-6 / Q000378:metabolism*; D051379:Mice; D009000:Monocytes / Q000378:metabolism*; D011565:Psoriasis / Q000139:chemically induced* / Q000378:metabolism*; D019947:Receptors, Interleukin-6 / Q000378:metabolism; D015398:Signal Transduction; D013154:Spleen / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000634:Aminoquinolines; D015850:Interleukin-6; D019947:Receptors, Interleukin-6; D000077271:Imiquimod