miR-181a Modulation of ERK-MAPK Signaling Sustains DC-SIGN Expression and Limits Activation of Monocyte-Derived Dendritic Cells

Clarice X. Lim, Bernett Lee, Olivia Geiger, Christina Passegger, Michaela Beitzinger, Johann Romberger, Anika Stracke, Christoph Högenauer, Anton Stift, Heribert Stoiber, Michael Poidinger, Armin Zebisch, Gunter Meister, Adam Williams, Richard A. Flavell, Jorge Henao-Mejia, Herbert Strobl*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

DC-SIGN+ mo-DCs play important roles in bacterial infections and inflammatory diseases, but the factors regulating differentiation and activation remain poorly defined. Lim et al. show that miR-181a simultaneously fine-tunes DC-SIGN+ mo-DC differentiation/activation by promoting ERK-MAPK signaling, which sustains DC-SIGN expression and limits its responsiveness to TLR4 triggering and inflammatory stimuli.

Original languageEnglish (US)
Pages (from-to)3793-3805.e5
JournalCell reports
Volume30
Issue number11
DOIs
StatePublished - Mar 17 2020

Keywords

  • DC-SIGN
  • DC-SIGN mo-DC
  • inflammation
  • miR-181a
  • mo-DC
  • monocyte-derived
  • terminal mo-DC differentiation
  • ulcerative colitis

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Fingerprint

Dive into the research topics of 'miR-181a Modulation of ERK-MAPK Signaling Sustains DC-SIGN Expression and Limits Activation of Monocyte-Derived Dendritic Cells'. Together they form a unique fingerprint.

Cite this