Agonistic Antibody to TLR4/MD-2 Protects Mice from Acute Lethal Hepatitis Induced by TNF-α | Zendy

Sachiko AkashiTakamura | Zendy; Takahisa Furuta | Zendy; Koichiro Takahashi | Zendy; Natsuko Tanimura | Zendy; Yutaka Kusumoto | Zendy; Toshihiko Kobayashi | Zendy; Shin-ichiroh Saitoh | Zendy; Yoshiyuki Adachi | Zendy; Takahiro Doi | Zendy; Kensuke Miyake | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Agonistic Antibody to TLR4/MD-2 Protects Mice from Acute Lethal Hepatitis Induced by TNF-α

Author(s) -

Sachiko AkashiTakamura,

Takahisa Furuta,

Koichiro Takahashi,

Natsuko Tanimura,

Yutaka Kusumoto,

Toshihiko Kobayashi,

Shin-ichiroh Saitoh,

Yoshiyuki Adachi,

Takahiro Doi,

Kensuke Miyake

Publication year - 2006

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.176.7.4244

Subject(s) - tlr4 , monoclonal antibody , tumor necrosis factor alpha , antibody , hepatitis , lipopolysaccharide , immunology , chemistry , inflammation , medicine , pharmacology , virology , microbiology and biotechnology , biology

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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research