scholarly journals Distinct CpG DNA and Polyinosinic-Polycytidylic Acid Double-Stranded RNA, Respectively, Stimulate CD11c−Type 2 Dendritic Cell Precursors and CD11c+Dendritic Cells to Produce Type I IFN

2001 ◽  
Vol 166 (4) ◽  
pp. 2291-2295 ◽  
Author(s):  
Norimitsu Kadowaki ◽  
Svetlana Antonenko ◽  
Yong-Jun Liu
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Type I ◽  
Type I Ifn ◽  
Cpg Dna ◽  
Double Stranded Rna ◽  
Polycytidylic Acid ◽  
Polyinosinic Polycytidylic Acid

scholarly journals Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection

2007 ◽  
Vol 81 (18) ◽  
pp. 9778-9789 ◽  
Author(s):  
Janet L. Weslow-Schmidt ◽  
Nancy A. Jewell ◽  
Sara E. Mertz ◽  
J. Pedro Simas ◽  
Joan E. Durbin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cell Activation ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
The Body ◽  
Type I ◽  
Type I Ifn ◽  
Dendritic Cell Activation ◽  
Murine Gammaherpesvirus

ABSTRACT The respiratory tract is a major mucosal site for microorganism entry into the body, and type I interferon (IFN) and dendritic cells constitute a first line of defense against viral infections. We have analyzed the interaction between a model DNA virus, plasmacytoid dendritic cells, and type I IFN during lung infection of mice. Our data show that murine gammaherpesvirus 68 (γHV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to γHV68. Following γHV68 intranasal inoculation, the local and systemic IFN-α/β response is below detectable levels, and plasmacytoid dendritic cells are activated and recruited into the lung with a tissue distribution that differs from that of conventional dendritic cells. Our results suggest that plasmacytoid dendritic cells and type I IFN have important but independent roles during the early response to a respiratory γHV68 infection. γHV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-α/β in vivo, which may serve as an immune evasion strategy.

scholarly journals Dendritic cells activated by double-stranded RNA induce arthritis via autocrine type I IFN signaling

2013 ◽  
Vol 95 (4) ◽  
pp. 661-666 ◽  
Author(s):  
S. C. Narendra ◽  
J. P. Chalise ◽  
N. Hook ◽  
M. Magnusson
Keyword(s):  
Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Double Stranded Rna ◽  
Induce Arthritis

scholarly journals Enhancement of Dendritic Cell Antigen Cross-Presentation by CpG DNA Involves Type I IFN and Stabilization of Class I MHC mRNA

2005 ◽  
Vol 175 (4) ◽  
pp. 2244-2251 ◽  
Author(s):  
John Kuchtey ◽  
Peter J. Chefalo ◽  
Reginald C. Gray ◽  
Lakshmi Ramachandra ◽  
Clifford V. Harding
Keyword(s):  
Dendritic Cell ◽  
Class I ◽  
Type I ◽  
Type I Ifn ◽  
Class I Mhc ◽  
Cpg Dna ◽  
Cell Antigen ◽  
Cross Presentation

scholarly journals A type I IFN–Flt3 ligand axis augments plasmacytoid dendritic cell development from common lymphoid progenitors

2013 ◽  
Vol 210 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
Yi-Ling Chen ◽  
Ting-Ting Chen ◽  
Li-Mei Pai ◽  
Joanna Wesoly ◽  
Hans A.R. Bluyssen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cell ◽  
Critical Role ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Flt3 Ligand ◽  
Lymphoid Progenitors

During infections and inflammation, plasmacytoid dendritic cells (pDCs) are the most potent type I interferon (IFN-I)–producing cells. However, the developmental origin of pDCs and the signals dictating pDC generation remain incompletely understood. Here, we report a synergistic role for IFN-I and Flt3 ligand (FL) in pDC development from common lymphoid progenitors (CLPs). Both conventional DCs (cDCs) and pDCs were generated from CLPs in response to FL, whereas pDC generation required higher concentrations of FL and concurrent IFN-I signaling. An absence of IFN-I receptor, impairment of IFN-I signaling, or neutralization of IFN-I significantly impeded pDC development from CLPs. Furthermore, FL induced IFN-I expression in CLPs, which in turn induced Flt3 up-regulation that facilitated survival and proliferation of CLPs, as well as their differentiation into pDCs. Collectively, these results define a critical role for the FL/IFN-I/Flt3 axis in pDC differentiation from CLPs.

scholarly journals SARS-CoV-2 induces human plasmacytoid pre-dendritic cell diversification via UNC93B and IRAK4

2020 ◽  
Author(s):  
Fanny Onodi ◽  
Lucie Bonnet-Madin ◽  
Laurent Meertens ◽  
Léa Karpf ◽  
Justine Poirot ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Dendritic Cell ◽  
Late Stage ◽  
Antiviral Immunity ◽  
Interferon Α ◽  
Type I ◽  
Type I Ifn ◽  
Ox40 Ligand ◽  
Immune Pathways

Several studies have analyzed antiviral immune pathways in late-stage severe COVID-19. However, the initial steps of SARS-CoV-2 antiviral immunity are poorly understood. Here, we have isolated primary SARS-CoV-2 viral strains, and studied their interaction with human plasmacytoid pre-dendritic cells (pDC), a key player in antiviral immunity. We show that pDC are not productively infected by SARS-CoV-2. However, they efficiently diversified into activated P1-, P2-, and P3-pDC effector subsets in response to viral stimulation. They expressed CD80, CD86, CCR7, and OX40 ligand at levels similar to influenza virus-induced activation. They rapidly produced high levels of interferon-α, interferon-λ1, IL-6, IP-10, and IL-8. All major aspects of SARS-CoV-2-induced pDC activation were inhibited by hydroxychloroquine. Mechanistically, SARS-CoV-2-induced pDC activation critically depended on IRAK4 and UNC93B1, as established using pDC from genetically deficient patients. Overall, our data indicate that human pDC are efficiently activated by SARS-CoV-2 particles and may thus contribute to type I IFN-dependent immunity against SARS-CoV-2 infection.

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