| Literature DB >> 16547261 |
Sachiko Akashi-Takamura1, Takahisa Furuta, Koichiro Takahashi, Natsuko Tanimura, Yutaka Kusumoto, Toshihiko Kobayashi, Shin-Ichiroh Saitoh, Yoshiyuki Adachi, Takahiro Doi, Kensuke Miyake.
Abstract
LPS is recognized by a heterodimer consisting of TLR4 and its coreceptor MD-2. LPS signal causes excessive inflammation and tissue damage. In this study, we show that a mAb to TLR4/MD-2 protected mice from acute lethal hepatitis caused by LPS/d-galactosamine. The protective effect of the mAb was not due to inhibition of LPS response, because serum TNF-alpha, which was induced by LPS and caused lethal hepatitis, was 10 times up-regulated by the mAb pretreatment. Moreover, this mAb induced antiapoptotic genes in liver in a TLR4/MD-2-dependent manner. These results demonstrated that an agonistic mAb to TLR4/MD-2 protected mice from LPS/d-galactosamine-induced acute lethal hepatitis by delivering a protective signal activating NF-kappaB through TLR4/MD-2.Entities:
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Year: 2006 PMID： 16547261 DOI： 10.4049/jimmunol.176.7.4244
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422