miR-22 Controls Irf8 mRNA Abundance and Murine Dendritic Cell Development

Li, Haiyan S.; Greeley, Nathaniel; Sugimoto, Naoshi; Liu, Yong Jun; Watowich, Stephanie S.

doi:10.1371/journal.pone.0052341

Cited by 33 publications

(25 citation statements)

References 63 publications

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“…Dendritic cells are key antigen presenting cells important to activate interferon expression by T and NK cells, and MiR-22 has been implicated in normal dendritic cell development, possibly through repression of the interferon response factor 8 (IRF8). 21 Furthermore, miR-22 has also been shown to be essential for bone marrow derived-DC and lung CD11c+ APC activation to endotoxin and other stimulants in a mechanism involving inappropriate induction of HDAC4. Indeed, impaired DC activation has been shown to interfere with cross stimulation of the TH17 response in a mouse model of emphysema 22 .…”

Section: Discussionmentioning

confidence: 99%

“…showed that miR-22 suppresses IRF5 and HMGB1, two factors important to activating an interferon-mediated pro-inflammatory response through NK-κB and IRF3 20 . MiR-22 overexpression enhances development of conventional dendritic cells (cDC) through suppression of the interferon response gene Irf8 , and miR-22 is required for DC activation of TH17 responses through direct inhibition of the histone deacetylase HDAC4 21, 22 . Importantly, miR-22 has also been implicated in erythroid maturation, as expression of miR-22 was found to correlate with increasingly mature states of erythroid maturation in ex vivo culture of human CD34 + and K562 cells 23 .…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

Kadmon

Landers

et al. 2017

Experimental Hematology

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MicroRNA-22 (miR-22) is a highly conserved microRNA that can regulate cell proliferation, oncogenesis, and cell maturation, especially during stress. In hematopoietic stem cells (HSCs) miR-22 has been reported to be involved in the regulation of key self-renewal factors including Tet2. Recent work demonstrates that miR-22 also participates in regulation of the interferon response, and expression profiling studies suggest that it is variably expressed at different stages in erythroid differentiation. We thus hypothesized that miR-22 regulates maturation of erythroid progenitors during stress hematopoiesis through its interaction with interferon. We compared the blood and bone marrow of wild type (WT) and miR-22-deficient mice at baseline and upon infectious challenge with systemic lymphochoriomeningitis (LCMV) virus. MiR-22-deficient mice maintained platelet counts better than WT mice during infection, but they showed significantly reduced red blood cells (RBC) and hemoglobin. Analysis of bone marrow progenitors demonstrated better overall survival and improved HSC homeostasis in infected miR-22-null mice compared to WT, attributable to a blunted interferon response to LCMV challenge in the miR-22-null mice. We found that miR-22 was exclusively expressed in stage II erythroid precursors and was downregulated upon infection in WT mice. Our results indicate that miR-22 promotes the interferon response to viral infection and that it functions at baseline as a brake to slow erythroid differentiation and maintain adequate erythroid potential. Impaired regulation of erythrogenesis in the absence of miR-22 can lead to anemia during infection.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice

Kadmon

Landers

et al. 2017

Experimental Hematology

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“…miR-22 is induced in progenitor cultures by GM-CSF and it targets Irf8 mRNA for post-transcriptional repression 235 . Overexpression of miR-22 during DC development promotes the expansion of CD11b + cDC populations at the expense of pDCs.…”

Section: Development Of Pdcsmentioning

confidence: 99%

The multifaceted biology of plasmacytoid dendritic cells

2015

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Plasmacytoid dendritic cells (pDCs) are a unique dendritic cell subset that specializes in the production of type I interferons (IFNs). pDCs promote antiviral immune responses and have been implicated in the pathogenesis of autoimmune diseases characterized by a type I IFN signature. However, pDCs can also induce tolerogenic immune responses. Here, we review recent progress from the field of pDC biology, focusing on: the molecular mechanisms that regulate pDC development and functions; the pathways involved in their sensing of pathogens and endogenous nucleic acids; the function of pDCs at mucosal sites; and their roles in infections, autoimmunity and cancer.

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“…miRNAs post-transcriptionally control gene expression by targeting mRNAs for degradation or translational repression, and have multiple roles in various biological processes and diseases. Several miRNAs are found to be involved in the regulation of DC maturation and differentiation, such as miR-155 [105,106], miR-27 [107], miR-148/ 152a [108], miR-22 [109], miR-146a [110], etc. Recently, we established comprehensive miRNomes analysis in bone marrow HSCs, bone marrow-derived immature DCs, mature DCs and especially in the IL-10/NO-producing regulatory DCs.…”

Section: Epigenetic Control Of DC Tolerancementioning

confidence: 99%