Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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U1 cells stimulated with the TLR8 agonist 3M-002 at 10 microM show a prominent activation of TLR-dependent genes as assessed by "Human toll-like Receptor PCR array pathway" over time

ABSTRACT: We investigated the effects of the TLR8 agonist 3M-002 on latently HIV infected U1 cells. We found a prominent upregulation of TLR-dependent genes. Notably, the TLR8 agonist resulted in a marked activation of HIV. We stimulated U1 cells for 6 or 10 hours with 3M-002 and subsequently harvested the cells, extracted total RNA. RNA was then used for quantifiying TLR-dependent gene upregulation using a commercial PCR array pathway

ORGANISM(S): Homo sapiens

SUBMITTER: Roberto Speck 

PROVIDER: E-GEOD-26469 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TLR8 activates HIV from latently infected cells of myeloid-monocytic origin directly via the MAPK pathway and from latently infected CD4+ T cells indirectly via TNF-α.

Schlaepfer Erika E   Speck Roberto F RF  

Journal of immunology (Baltimore, Md. : 1950) 20110228 7

We previously showed that the TLR7/8 agonist, R-848, activated HIV from cells of myeloid-monocytic origin. In this work, we show that this effect was solely due to triggering TLR8 and that NF-κB was involved in the TLR8-mediated activation of HIV from latently infected cells of myeloid-monocytic origin. Inhibition of Erk1/2 or p38α resulted in attenuation of TLR8-mediated activation of NF-κB. Western blots confirmed that TLR8 triggering activated Erk1/2 and p38α but, surprisingly, not JNK. Altho  ...[more]

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