Susceptibility of human dendritic cells (DCs) to measles virus (MV) depends on their activation stages in conjunction with the level of CDw150: role of Toll stimulators in DC maturation and MV amplification

Murabayashi, Nozomu; Kurita-Taniguchi, Mitsue; Ayata, Minoru; Matsumoto, Misako; Ogura, Hisashi; Seya, Tsukasa

doi:10.1016/s1286-4579(02)01598-8

Cited by 44 publications

(43 citation statements)

References 47 publications

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“…In accordance with some previous data 43,44 , DCs generated from human monocytes expressed CD150 (Figure 5a). This expression was slightly increased after 24 h co-culture with CHO cells, presumably due to further DC maturation, as reflected by elevation of CD83 and HLA-DR expression and p38MAPK activation.…”

Section: Discussionsupporting

confidence: 93%

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

et al. 2015

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Measles virus (MV) is highly contagious pathogen, which causes a profound immunosuppression, resulting in high infant mortality. This virus infects dendritic cells (DCs) following the binding of MV hemagglutinin (MV-H) to CD150 receptor and alters DC functions by a mechanism that is not completely understood. We have analyzed the effect of MV-H interaction with CD150-expressing DCs on the DC signaling pathways and consequent phenotypic and functional changes in the absence of infectious context. We demonstrated that contact between CD150 on human DCs and MV-H expressed on membrane of transfected CHO cells was sufficient to modulate the activity of two major regulatory pathways of DC differentiation and function: to stimulate Akt and inhibit p38 MAPK phosphorylation, without concomitant ERK1/2 activation. Furthermore, interaction with MV-H decreased the expression level of DC activation markers CD80, CD83, CD86, and HLA-DR and strongly downregulated IL-12 production but did not modulate IL-10 secretion. Moreover, contact with MV-H suppressed DC-mediated T-cell alloproliferation, demonstrating profound alteration of DC maturation and functions. Finally, engagement of CD150 by MV-H in mice transgenic for human CD150 decreased inflammatory responses, showing the immunosuppressive effect of CD150-MV-H interaction in vivo. Altogether, these results uncover novel mechanism of MV-induced immunosuppression, implicating modulation of cell signaling pathways following MV-H interaction with CD150-expressing DCs and reveal anti-inflammatory effects of CD150 stimulation.

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Section: Discussionsupporting

confidence: 93%

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

et al. 2015

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“…The H glycoprotein is a determinant of MV infection of DCs (36) and can bind to Toll-like receptor-2 on macrophages (44) and to the MV receptors CD46 and SLAM (45). DCs express CD46 and increasing amounts of SLAM with differentiation (45), and the Chicago-1 strain of MV can use both receptors. In addition, the MV nucleocapsid can directly activate the IRF3 pathway intracellularly (46).…”

Section: Discussionmentioning

confidence: 99%

Gene expression patterns in dendritic cells infected with measles virus compared with other pathogens

Zilliox

Parmigiani

Griffin

2006

Proc. Natl. Acad. Sci. U.S.A.

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Gene expression patterns supply insight into complex biological networks that provide the organization in which viruses and host cells interact. Measles virus (MV) is an important human pathogen that induces transient immunosuppression followed by life-long immunity in infected individuals. Dendritic cells (DCs) are potent antigen-presenting cells that initiate the immune response to pathogens and are postulated to play a role in MV-induced immunosuppression. To better understand the interaction of MV with DCs, we examined the gene expression changes that occur over the first 24 h after infection and compared these changes to those induced by other viral, bacterial, and fungal pathogens. There were 1,553 significantly regulated genes with nearly 60% of them down-regulated. MV-infected DCs up-regulated a core of genes associated with maturation of antigen-presenting function and migration to lymph nodes but also included genes for IFN-regulatory factors 1 and 7, 2 5 oligoadenylate synthetase, Mx, and TNF superfamily proteins 2, 7, 9, and 10 (TNF-related apoptosisinducing ligand). MV induced genes for IFNs, ILs, chemokines, antiviral proteins, histones, and metallothioneins, many of which were also induced by influenza virus, whereas genes for protein synthesis and oxidative phosphorylation were down-regulated. Unique to MV were the induction of genes for a broad array of IFN-␣s and the failure to up-regulate dsRNA-dependent protein kinase. These results provide a modular view of common and unique DC responses after infection and suggest mechanisms by which MV may modulate the immune response.immunosuppression ͉ IFN ͉ microarray ͉ dsRNA-dependent protein kinase

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“…Ichinose (IC)-B was provided from Dr. F. Kobune (National Institutes of Health, Tokyo, Japan) (Kubune et al, 1990). Masusako (MS) was propagated in our laboratory (Kurita-Taniguchi et al, 2000;Murabayashi et al, 2002). NV, ED and MS strains were maintained in Vero/CD150 cells in our laboratory (Shingai et al, 2007).…”

Section: Virus Preparation and Titrationmentioning

confidence: 99%

Strain-to-strain difference of V protein of measles virus affects MDA5-mediated IFN-β-inducing potential

Takaki

Watanabe

Shingai

et al. 2011

Molecular Immunology

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Laboratory-adapted and vaccine strains of measles virus (MV) induce type I interferon (IFN) in infected cells to a far greater extent than wild-type strains. We investigated the mechanisms for this differential type I IFN production in cells infected with representative MV strains. The overexpression of the wild-type V protein suppressed melanoma differentiation-associated gene 5 (MDA5)-induced IFN-E promoter activity, while this was not seen in A549 cells expressing CD150 infected with the V protein of the vaccine strain. The V proteins of the wild-type also suppressed poly I:C-induced IFN regulatory factor 3 (IRF-3) dimerization. The V proteins of the wild-type and vaccine strain did not affect retinoic acid-inducible gene 1 (RIG-I)-or toll-IL-1R homology domain-containing adaptor molecule 1 (TICAM-1)-induced IFN-E promoter activation. We identified an amino acid substitution of the cysteine residue at position 272 (which is conserved among paramyxoviruses) to an arginine residue in the V protein of the vaccine strain. Only the V protein possessing the 272C residue binds to MDA5. The mutation introduced into the wild-type V protein (C272R) was unable to suppress MDA5-induced IRF-3 nuclear translocation and IFN-E promoter activation as seen in the V proteins of the vaccine strain, whereas the mutation introduced in the vaccine strain V protein (R272C) was able to inhibit MDA5-induced IRF-3 and IFN-E promoter activation. The other 6 residues of the vaccine strain V sequence inconsistent with the authentic sequence of the wild-type V protein barely affected the IRF-3 nuclear translocation. These data suggested that the structural difference of vaccine MV V protein hampers MDA5 blockade and acts as a nidus for the spread/amplification of type I IFN induction. Ultimately, measles vaccine strains have two modes of IFN-E-induction for their attenuation: V protein mutation and production of defective interference (DI) RNA.3

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Susceptibility of human dendritic cells (DCs) to measles virus (MV) depends on their activation stages in conjunction with the level of CDw150: role of Toll stimulators in DC maturation and MV amplification

Cited by 44 publications

References 47 publications

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

Measles virus hemagglutinin triggers intracellular signaling in CD150-expressing dendritic cells and inhibits immune response

Gene expression patterns in dendritic cells infected with measles virus compared with other pathogens

Strain-to-strain difference of V protein of measles virus affects MDA5-mediated IFN-β-inducing potential

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