2. Other local factors clearly existed, such as pancreatitis or splenectomy. 3. Cirrhosis was in a compensated condition. In reverse, PVT with well-compensated cirrhosis should not be excluded from noncirrhotic PVT. The effect can be better only if we aim at the major etiology more accurately and
Toll-like receptors and adaptor molecules in liver disease: Update
β Scribed by Ekihiro Seki; David A. Brenner
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 705 KB
- Volume
- 48
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ Synopsis
Toll-like receptors (TLRs) are pattern recognition receptors that recognize pathogen-associated molecular patterns and signal through adaptor molecules, myeloid differentiation factor 88 (MyD88), Toll/IL-1 receptor domain containing adaptor protein (TIRAP), Toll/IL-1 receptor domain containing adaptor inducing interferon-beta (TRIF), and TRIF-related adaptor molecule (TRAM) to activate transcription factors, nuclear factor (NF)-kappaB, activator protein 1 (AP-1), and interferon regulatory factors (IRFs) leading to the initiation of innate immunity. This system promptly initiates host defenses against invading microorganisms. Endogenous TLR ligands such as the products from dying cells may also engage with TLRs as damage-associated molecular patterns. Although Kupffer cells are considered the primary cells to respond to pathogen associated molecular patterns in the liver, recent studies provide evidence of TLR signaling in hepatic nonimmune cell populations, including hepatocytes, biliary epithelial cells, endothelial cells, and hepatic stellate cells. This review highlights advances in TLR signaling in the liver, the role of TLRs in the individual hepatic cell populations, and the implication of TLR signaling in acute and chronic liver diseases. We further discuss recent advances regarding cytosolic pattern recognition receptors, RNA helicases that represents a new concept in chronic hepatitis C virus infection.
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