scholarly journals Selective blockade of the inhibitory Fcγ receptor (FcγRIIB) in human dendritic cells and monocytes induces a type I interferon response program

2007 ◽  
Vol 204 (10) ◽  
pp. 2489-2489 ◽  
Author(s):  
Kavita M. Dhodapkar ◽  
Devi Banerjee ◽  
John Connolly ◽  
Anjli Kukreja ◽  
Elyana Matayeva ◽  
...  

2007 ◽  
Vol 204 (10) ◽  
pp. 2494-2494
Author(s):  
Kavita M. Dhodapkar ◽  
Devi Banerjee ◽  
John Connolly ◽  
Anjli Kukreja ◽  
Elyana Matayeva ◽  
...  


2007 ◽  
Vol 204 (6) ◽  
pp. 1359-1369 ◽  
Author(s):  
Kavita M. Dhodapkar ◽  
Devi Banerjee ◽  
John Connolly ◽  
Anjli Kukreja ◽  
Elyana Matayeva ◽  
...  

The ability of dendritic cells (DCs) to activate immunity is linked to their maturation status. In prior studies, we have shown that selective antibody-mediated blockade of inhibitory FcγRIIB receptor on human DCs in the presence of activating immunoglobulin (Ig) ligands leads to DC maturation and enhanced immunity to antibody-coated tumor cells. We show that Fcγ receptor (FcγR)–mediated activation of human monocytes and monocyte-derived DCs is associated with a distinct gene expression pattern, including several inflammation-associated chemokines, as well as type 1 interferon (IFN) response genes, including the activation of signal transducer and activator of transcription 1 (STAT1). FcγR-mediated STAT1 activation is rapid and requires activating FcγRs. However, this IFN response is observed without a detectable increase in the expression of type I IFNs themselves or the need to add exogenous IFNs. Induction of IFN response genes plays an important role in FcγR-mediated effects on DCs, as suppression of STAT1 by RNA interference inhibited FcγR-mediated DC maturation. These data suggest that the balance of activating/inhibitory FcγRs may regulate IFN signaling in myeloid cells. Manipulation of FcγR balance on DCs and monocytes may provide a novel approach to regulating IFN-mediated pathways in autoimmunity and human cancer.



2011 ◽  
Vol 85 (22) ◽  
pp. 12093-12097 ◽  
Author(s):  
X. Carnec ◽  
S. Baize ◽  
S. Reynard ◽  
L. Diancourt ◽  
V. Caro ◽  
...  


2010 ◽  
Vol 84 (19) ◽  
pp. 9760-9774 ◽  
Author(s):  
Juan R. Rodriguez-Madoz ◽  
Alan Belicha-Villanueva ◽  
Dabeiba Bernal-Rubio ◽  
Joseph Ashour ◽  
Juan Ayllon ◽  
...  

ABSTRACT Dengue virus (DENV) is the most prevalent arthropod-borne human virus, able to infect and replicate in human dendritic cells (DCs), inducing their activation and the production of proinflammatory cytokines. However, DENV can successfully evade the immune response in order to produce disease in humans. Several mechanisms of immune evasion have been suggested for DENV, most of them involving interference with type I interferon (IFN) signaling. We recently reported that DENV infection of human DCs does not induce type I IFN production by those infected DCs, impairing their ability to prime naive T cells toward Th1 immunity. In this article, we report that DENV also reduces the ability of DCs to produce type I IFN in response to several inducers, such as infection with other viruses or exposure to Toll-like receptor (TLR) ligands, indicating that DENV antagonizes the type I IFN production pathway in human DCs. DENV-infected human DCs showed a reduced type I IFN response to Newcastle disease virus (NDV), Sendai virus (SeV), and Semliki Forest virus (SFV) infection and to the TLR3 agonist poly(I:C). This inhibitory effect is DENV dose dependent, requires DENV replication, and takes place in DENV-infected DCs as early as 2 h after infection. Expressing individual proteins of DENV in the presence of an IFN-α/β production inducer reveals that a catalytically active viral protease complex is required to reduce type I IFN production significantly. These results provide a new mechanism by which DENV evades the immune system in humans.



2018 ◽  
Vol 9 ◽  
Author(s):  
Tünde Fekete ◽  
Dora Bencze ◽  
Attila Szabo ◽  
Eszter Csoma ◽  
Tamas Biro ◽  
...  


2011 ◽  
Vol 85 (6) ◽  
pp. 3042-3042
Author(s):  
J. R. Rodriguez-Madoz ◽  
D. Bernal-Rubio ◽  
D. Kaminski ◽  
K. Boyd ◽  
A. Fernandez-Sesma


2012 ◽  
Vol 42 (3) ◽  
pp. 573-579 ◽  
Author(s):  
Eiji Esashi ◽  
Musheng Bao ◽  
Yi-Hong Wang ◽  
Wei Cao ◽  
Yong-Jun Liu


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