IL-6 Signaling in Myelomonocytic Cells Is Not Crucial for the Development of IMQ-Induced Psoriasis

PLoS One. 2016 Mar 21;11(3):e0151913. doi: 10.1371/journal.pone.0151913. eCollection 2016.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aminoquinolines / adverse effects*
  • Animals
  • Bone Marrow / pathology
  • Cell Compartmentation
  • Gene Deletion
  • Humans
  • Imiquimod
  • Interleukin-6 / metabolism*
  • Mice
  • Monocytes / metabolism*
  • Psoriasis / chemically induced*
  • Psoriasis / metabolism*
  • Receptors, Interleukin-6 / metabolism
  • Signal Transduction*
  • Spleen / pathology
  • T-Lymphocytes / immunology

Substances

  • Aminoquinolines
  • Interleukin-6
  • Receptors, Interleukin-6
  • Imiquimod

Grants and funding

Research was supported by the German Research Foundation (DFG) grants CRC/TRR 156 (TPC01) to AW and KA 4035/1-1 to SHK. SHK research was also supported by the Stiftung Mainzer Herz and the program MAIFOR from the University of Mainz. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.