Cutting edge: ABIN-1 protects against psoriasis by restricting MyD88 signals in dendritic cells

J Immunol. 2013 Jul 15;191(2):535-9. doi: 10.4049/jimmunol.1203335. Epub 2013 Jun 19.

Abstract

Psoriasis is a chronic, inflammatory skin disease caused by a combination of environmental and genetic factors. The Tnip1 gene encodes A20 binding and inhibitor of NF-κB-1 (ABIN-1) protein and is strongly associated with susceptibility to psoriasis in humans. ABIN-1, a widely expressed ubiquitin-binding protein, restricts TNF- and TLR-induced signals. In this study, we report that mice lacking ABIN-1 specifically in dendritic cells (DCs), ABIN-1(fl) CD11c-Cre mice, exhibit perturbed immune homeostasis. ABIN-1-deficient DCs display exaggerated NF-κB and MAPK signaling and produce more IL-23 than do normal cells in response to TLR ligands. Challenge of ABIN-1(fl) CD11c-Cre mice with topical TLR7 ligand leads to greater numbers of Th17 and TCRγδ T cells and exacerbated development of psoriaform lesions. These phenotypes are reversed by DC-specific deletion of the TLR adaptor MyD88. These studies link ABIN-1 with IL-23 and IL-17, and they provide cellular and molecular mechanisms by which ABIN-1 regulates susceptibility to psoriasis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing / deficiency
  • Adaptor Proteins, Signal Transducing / genetics*
  • Adaptor Proteins, Signal Transducing / physiology*
  • Animals
  • Cells, Cultured
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism*
  • Disease Susceptibility
  • Inflammation
  • Interleukin-17 / metabolism*
  • Interleukin-23 / metabolism*
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitogen-Activated Protein Kinases / metabolism
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / metabolism*
  • NF-kappa B / metabolism
  • Psoriasis / genetics
  • Psoriasis / immunology*
  • Psoriasis / metabolism
  • Signal Transduction
  • Th17 Cells / immunology
  • Toll-Like Receptor 7 / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Interleukin-17
  • Interleukin-23
  • Membrane Glycoproteins
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Tlr7 protein, mouse
  • Tnip2 protein, mouse
  • Toll-Like Receptor 7
  • Mitogen-Activated Protein Kinases