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Seoul virus suppresses NF-κB-mediated inflammatory responses of antigen presenting cells from Norway rats
被引:18
作者:
Au, Rebecca Y.
[1
]
Jedlicka, Anne E.
[1
]
Li, Wei
[1
]
Pekosz, Andrew
[1
]
Klein, Sabra L.
[1
,2
]
机构:
[1] Johns Hopkins Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA
[2] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biochem & Mol Biol, Baltimore, MD 21205 USA
来源:
关键词:
Dendritic cells;
Hantavirus;
Innate immunity;
Interferon;
Macrophage;
MHC;
Rodent;
Toll-like receptor;
TNF;
Vital persistence;
HANTAVIRUS PULMONARY SYNDROME;
NECROSIS-FACTOR-ALPHA;
SIN-NOMBRE-VIRUS;
ENDOTHELIAL-CELLS;
HEMORRHAGIC-FEVER;
NONPATHOGENIC HANTAVIRUSES;
RENAL SYNDROME;
DENDRITIC CELLS;
HUMAN MONOCYTES;
TGF-BETA;
D O I:
10.1016/j.virol.2010.01.027
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
Hantavirus infection reduces antiviral defenses, increases regulatory responses, and causes persistent infection in rodent hosts. To address whether hantaviruses alter the Maturation and functional activity of antigen presenting cells (APCs), rat bone marrow-derived dendritic cells (BMDCs) and macrophages (BMDMs) were generated and infected with Seoul Virus (SEOV) or stimulated with TLR ligands. SEOV infected both DCs and macrophages, but copies of viral RNA, viral antigen, and infectious virus titers were higher in macrophages. The expression of MHCII and CD80, production of IL-6, IL-10, and TNF-alpha, and expression of Ifn beta were attenuated in SEOV-infected APCs. Stimulation of APCs with poly I:C prior to SEOV infection increased the expression of activation markers and production of inflammatory cytokines and suppressed SEOV replication. Infection of APCs with SEOV Suppressed LPS-induced activation and innate immune responses. Hantaviruses reduce the innate immune response potential of APCs derived from a natural host, which may influence persistence of these zoonotic viruses in the environment. (C) 2010 Elsevier Inc. All rights reserved.
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页码:115 / 127
页数:13
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