| First Author | Akashi-Takamura S | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 7 | Pages | 4244-51 |
| PubMed ID | 16547261 | Mgi Jnum | J:129909 |
| Mgi Id | MGI:3770373 | Doi | 10.4049/jimmunol.176.7.4244 |
| Citation | Akashi-Takamura S, et al. (2006) Agonistic antibody to TLR4/MD-2 protects mice from acute lethal hepatitis induced by TNF-alpha. J Immunol 176(7):4244-51 |
| abstractText | 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. |
