Cutting edge: MicroRNA-223 regulates myeloid dendritic cell-driven Th17 responses in experimental autoimmune encephalomyelitis

Igal Ifergan, Siqi Chen, Bin Zhang, Stephen D. Miller*

*Corresponding author for this work

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

Myeloid cells play a crucial role in the induction and sustained inflammation in neuroinflammatory disorders, such as multiple sclerosis. miR-223, a myeloid cell-specific microRNA, is one of the most upregulated microRNAs in multiple sclerosis patients. We demonstrate that miR-223-knockout mice display significantly reduced active and adoptive-transfer experimental autoimmune encephalomyelitis that is characterized by reduced numbers of myeloid dendritic cells (mDCs) and Th17 cells in the CNS. Knockout mDCs have increased PD-L1 and decreased IL-1b, IL-6, and IL-23 expression, as well as a reduced capacity to drive Th17, but not Th1, cell differentiation. Thus, miR-223 controls mDC-induced activation of pathologic Th17 responses during autoimmune inflammation.

Original languageEnglish (US)
Pages (from-to)1455-1459
Number of pages5
JournalJournal of Immunology
Volume196
Issue number4
DOIs
StatePublished - Feb 15 2016

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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