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Nat Immunol. 2014 Jan;15(1):54-62. doi: 10.1038/ni.2767. Epub 2013 Nov 24.

The miR-126-VEGFR2 axis controls the innate response to pathogen-associated nucleic acids.

Author information

1
Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
2
1] Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA. [2] Mount Sinai Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
3
Department of Biochemistry, State University of New York at Buffalo, Buffalo, New York, USA.
4
1] Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA. [2] Mount Sinai Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Abstract

miR-126 is a microRNA expressed predominately by endothelial cells and controls angiogenesis. We found miR-126 was required for the innate response to pathogen-associated nucleic acids and that miR-126-deficient mice had greater susceptibility to infection with pseudotyped HIV. Profiling of miRNA indicated that miR-126 had high and specific expression by plasmacytoid dendritic cells (pDCs). Moreover, miR-126 controlled the survival and function of pDCs and regulated the expression of genes encoding molecules involved in the innate response, including Tlr7, Tlr9 and Nfkb1, as well as Kdr, which encodes the growth factor receptor VEGFR2. Deletion of Kdr in DCs resulted in reduced production of type I interferon, which supports the proposal of a role for VEGFR2 in miR-126 regulation of pDCs. Our studies identify the miR-126-VEGFR2 axis as an important regulator of the innate response that operates through multiscale control of pDCs.

PMID:
24270517
PMCID:
PMC3896265
DOI:
10.1038/ni.2767
[Indexed for MEDLINE]
Free PMC Article

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