kelly to CO-CURE May 16
Virol J. 2010 May 10;7(1):91. [Epub ahead of print] (virology link)
*Human herpesvirus 6 infection impairs Toll-like receptor signaling**.* (ncbi link)
Murakami Y, Tanimoto K, Fujiwara H, An J, Suemori K, Ochi T, Hasegawa H, Yasukawa M.
*Abstract*
ABSTRACT: Human herpesvirus 6 (HHV-6) has a tropism for immunocompetent
cells, including T lymphocytes, monocytes/macrophages, and dendritic cells
(DCs) suggesting that HHV-6 infection affects the immunosurveillance system.
Toll-like receptor (TLR) system plays an important role in innate immunity
against various pathogens.
In the present study, we investigated the effect of HHV-6 infection on the
expression and intracellular signaling of TLRs in DCs.
Although expression levels of TLRs were not decreased or slightly elevated
following HHV-6 infection, the amounts of cytokines produced following
stimulation with ligands for TLRs appeared to be dramatically decreased in
HHV-6-infected DCs as compared to mock-infected DCs. Similarly,
phosphorylation levels of TAK-1, IkB kinase, and IkB-a following stimulation
of HHV-6-infected DCs with lipopolysaccharide, which is the ligand for TLR4,
appeared to be decreased.
These data show that HHV-6 impairs intracellular signaling through TLRs
indicating the novel mechanism of HHV-6-mediated immunomodulation.
http://www.virologyj.com/content/7/1/91
Virol J. 2010 May 10;7(1):91. [Epub ahead of print] (virology link)
*Human herpesvirus 6 infection impairs Toll-like receptor signaling**.* (ncbi link)
Murakami Y, Tanimoto K, Fujiwara H, An J, Suemori K, Ochi T, Hasegawa H, Yasukawa M.
*Abstract*
ABSTRACT: Human herpesvirus 6 (HHV-6) has a tropism for immunocompetent
cells, including T lymphocytes, monocytes/macrophages, and dendritic cells
(DCs) suggesting that HHV-6 infection affects the immunosurveillance system.
Toll-like receptor (TLR) system plays an important role in innate immunity
against various pathogens.
In the present study, we investigated the effect of HHV-6 infection on the
expression and intracellular signaling of TLRs in DCs.
Although expression levels of TLRs were not decreased or slightly elevated
following HHV-6 infection, the amounts of cytokines produced following
stimulation with ligands for TLRs appeared to be dramatically decreased in
HHV-6-infected DCs as compared to mock-infected DCs. Similarly,
phosphorylation levels of TAK-1, IkB kinase, and IkB-a following stimulation
of HHV-6-infected DCs with lipopolysaccharide, which is the ligand for TLR4,
appeared to be decreased.
These data show that HHV-6 impairs intracellular signaling through TLRs
indicating the novel mechanism of HHV-6-mediated immunomodulation.
http://www.virologyj.com/content/7/1/91