859 Analysis of Classe Ii Hla in Patients With Chronic Hepatitis C With Characteristics of Autoimmune Hepatitis

Tani, Claudia Megumi; Abrantes-Lemos, C.P.; Nakhle, Maria Cristina; Preuhs-Filho, G.; Rodrigues, H.; Deguti, Marta Mitiko; Kalil, J.; Carrilho, F.; Cancado, E. L. R.

doi:10.1016/s0168-8278(08)60861-2

Cited by 1 publication

(6 citation statements)

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“…Hepatocytes may uptake and remove endotoxin derived from the intestine through portal circulation (Seki and Brenner, 2008). Primary cultured hepatocytes express mRNA for all TLRs, but the expression levels are very low.…”

Section: Tlr Expression In the Livermentioning

confidence: 99%

“…Primary cultured hepatocytes express mRNA for all TLRs, but the expression levels are very low. While cultured hepatocytes respond to TLR2 and TLR4 ligands, their responses in vivo are quite weak (Isogawa et al, 2005; Seki and Brenner, 2008). …”

Section: Tlr Expression In the Livermentioning

confidence: 99%

“…Kupffer cells are the primary cells that encounter the gut-derived toxins such as LPS, but are less responsiveness due to “LPS tolerance” that prevents overt inflammation in the physiological setting (Seki and Brenner, 2008). Kupffer cells respond to all TLR ligands to produce TNF-α, IL-1, IL-6, IL-12, IL-18, and IL-10 (Seki et al, 2001; Wu et al, 2010).…”

Section: Tlr Expression In the Livermentioning

confidence: 99%

“…Amongst these events, the hepatic innate immune system plays a critical role and is activated in both acute and chronic liver diseases (Seki and Brenner, 2008; Seki and Schnabl, 2012). The healthy intestine prevents the translocation of intestine-derived microbial products by intact barrier system.…”

Section: Introductionmentioning

confidence: 99%

“…Accumulated lines of evidence indicate that TLRs are also activated by endogenous ligands, such as high mobility group box 1 (HMGB1), hyaluronan, and heat shock proteins released from damaged tissues, termed damaged associated molecular patterns (DAMPs; Takeuchi and Akira, 2010; Yamamoto and Takeda, 2010). In addition, innate immune response contributes not only to liver inflammation, but also to physiological and pathological repair processes including liver fibrosis, regeneration, and carcinogenesis (Seki and Brenner, 2008; Guo and Friedman, 2010; Seki and Schnabl, 2012). This review focuses on the current knowledge of TLRs, their ligands, intracellular signaling and cells expressing TLRs in liver fibrosis and its associated diseases, such as viral hepatitis, non-alcoholic and alcoholic steatohepatitis, primary biliary cirrhosis, and cystic fibrosis (CF).…”

Section: Introductionmentioning

confidence: 99%

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Toll-Like Receptors in Liver Fibrosis: Cellular Crosstalk and Mechanisms

Yang¹,

Seki²

2012

Front. Physio.

140

139

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Toll-like receptors (TLRs) are pattern recognition receptors that distinguish conserved microbial products, also known as pathogen-associated molecular patterns (PAMPs), from host molecules. Liver is the first filter organ between the gastrointestinal tracts and the rest of the body through portal circulation. Thus, the liver is a major organ that must deal with PAMPs and microorganisms translocated from the intestine and to respond to the damage associated molecular patterns (DAMPs) released from injured organs. These PAMPs and DAMPs preferentially activate TLR signaling on various cell types in the liver inducing the production of inflammatory and fibrogenic cytokines that initiate and prolong liver inflammation, thereby leading to fibrosis. We summarize recent findings on the role of TLRs, ligands, and intracellular signaling in the pathophysiology of liver fibrosis due to different etiology, as well as to highlight the potential role of TLR signaling in liver fibrosis associated with hepatitis C infection, non-alcoholic and alcoholic steatoheoatitis, primary biliary cirrhosis, and cystic fibrosis.

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Section: Tlr Expression In the Livermentioning

confidence: 99%

Section: Tlr Expression In the Livermentioning

confidence: 99%