FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2288573834> ?p ?o ?g. }

• W2288573834 endingPage "1127" @default.
• W2288573834 startingPage "1118" @default.
• W2288573834 abstract "Background & AimsMucosal-Associated Invariant T (MAIT) cells are innate-like T cells characterised by the invariant TCR-chain, Vα7.2-Jα33, and are restricted by MR1, which presents bacterial vitamin B metabolites. They are important for antibacterial immunity at mucosal sites; however, detailed characteristics of liver-infiltrating MAIT (LI-MAIT) and their role in biliary immune surveillance remain unexplored.MethodsThe phenotype and intrahepatic localisation of human LI-MAIT cells was examined in diseased and normal livers. MAIT cell activation in response to E. coli-exposed macrophages, biliary epithelial cells (BEC) and liver B cells was assessed with/without anti-MR1.ResultsIntrahepatic MAIT cells predominantly localised to bile ducts in the portal tracts. Consistent with this distribution, they expressed biliary tropic chemokine receptors CCR6, CXCR6, and integrin αEβ7. LI-MAIT cells were also present in the hepatic sinusoids and possessed tissue-homing chemokine receptor CXCR3 and integrins LFA-1 and VLA-4, suggesting their recruitment via hepatic sinusoids. LI-MAIT cells were enriched in the parenchyma of acute liver failure livers compared to chronic diseased livers. LI-MAIT cells had an activated, effector memory phenotype, expressed α4β7 and receptors for IL-12, IL-18, and IL-23. Importantly, in response to E. coli-exposed macrophages, liver B cells and BEC, MAIT cells upregulated IFN-γ and CD40 Ligand and degranulated in an MR1-dependent, cytokine-independent manner. In addition, diseased liver MAIT cells expressed T-bet and RORγt and the cytokines IFN-γ, TNF-α, and IL-17.ConclusionsOur findings provide the first evidence of an immune surveillance effector response for MAIT cells towards BEC in human liver; thus they could be manipulated for treatment of biliary disease in the future. Mucosal-Associated Invariant T (MAIT) cells are innate-like T cells characterised by the invariant TCR-chain, Vα7.2-Jα33, and are restricted by MR1, which presents bacterial vitamin B metabolites. They are important for antibacterial immunity at mucosal sites; however, detailed characteristics of liver-infiltrating MAIT (LI-MAIT) and their role in biliary immune surveillance remain unexplored. The phenotype and intrahepatic localisation of human LI-MAIT cells was examined in diseased and normal livers. MAIT cell activation in response to E. coli-exposed macrophages, biliary epithelial cells (BEC) and liver B cells was assessed with/without anti-MR1. Intrahepatic MAIT cells predominantly localised to bile ducts in the portal tracts. Consistent with this distribution, they expressed biliary tropic chemokine receptors CCR6, CXCR6, and integrin αEβ7. LI-MAIT cells were also present in the hepatic sinusoids and possessed tissue-homing chemokine receptor CXCR3 and integrins LFA-1 and VLA-4, suggesting their recruitment via hepatic sinusoids. LI-MAIT cells were enriched in the parenchyma of acute liver failure livers compared to chronic diseased livers. LI-MAIT cells had an activated, effector memory phenotype, expressed α4β7 and receptors for IL-12, IL-18, and IL-23. Importantly, in response to E. coli-exposed macrophages, liver B cells and BEC, MAIT cells upregulated IFN-γ and CD40 Ligand and degranulated in an MR1-dependent, cytokine-independent manner. In addition, diseased liver MAIT cells expressed T-bet and RORγt and the cytokines IFN-γ, TNF-α, and IL-17. Our findings provide the first evidence of an immune surveillance effector response for MAIT cells towards BEC in human liver; thus they could be manipulated for treatment of biliary disease in the future." @default.
• W2288573834 created "2016-06-24" @default.
• W2288573834 creator A5001501626 @default.
• W2288573834 creator A5003824543 @default.
• W2288573834 creator A5003995610 @default.
• W2288573834 creator A5004309561 @default.
• W2288573834 creator A5005888483 @default.
• W2288573834 creator A5010503980 @default.
• W2288573834 creator A5019716566 @default.
• W2288573834 creator A5022140384 @default.
• W2288573834 creator A5024685746 @default.
• W2288573834 creator A5029540094 @default.
• W2288573834 creator A5029546143 @default.
• W2288573834 creator A5031311628 @default.
• W2288573834 creator A5049631280 @default.
• W2288573834 creator A5051886419 @default.
• W2288573834 creator A5052881818 @default.
• W2288573834 creator A5057244422 @default.
• W2288573834 creator A5073689179 @default.
• W2288573834 creator A5084623065 @default.
• W2288573834 date "2016-05-01" @default.
• W2288573834 modified "2023-10-06" @default.
• W2288573834 title "Biliary epithelium and liver B cells exposed to bacteria activate intrahepatic MAIT cells through MR1" @default.
• W2288573834 cites W1487816967 @default.
• W2288573834 cites W1490413060 @default.
• W2288573834 cites W1538607209 @default.
• W2288573834 cites W1554432738 @default.
• W2288573834 cites W1659107174 @default.
• W2288573834 cites W1875741133 @default.
• W2288573834 cites W1935043882 @default.
• W2288573834 cites W1981006861 @default.
• W2288573834 cites W1981700081 @default.
• W2288573834 cites W1982688638 @default.
• W2288573834 cites W1990432039 @default.
• W2288573834 cites W2004071897 @default.
• W2288573834 cites W2006188503 @default.
• W2288573834 cites W2009031590 @default.
• W2288573834 cites W2011770661 @default.
• W2288573834 cites W2013097614 @default.
• W2288573834 cites W2027160668 @default.
• W2288573834 cites W2030817385 @default.
• W2288573834 cites W2031457861 @default.
• W2288573834 cites W2037271656 @default.
• W2288573834 cites W2037555606 @default.
• W2288573834 cites W2040423355 @default.
• W2288573834 cites W2042172298 @default.
• W2288573834 cites W2044963057 @default.
• W2288573834 cites W2049739427 @default.
• W2288573834 cites W2051787179 @default.
• W2288573834 cites W2058739008 @default.
• W2288573834 cites W2065252029 @default.
• W2288573834 cites W2068487285 @default.
• W2288573834 cites W2073247934 @default.
• W2288573834 cites W2074860415 @default.
• W2288573834 cites W2088380096 @default.
• W2288573834 cites W2095128898 @default.
• W2288573834 cites W2098258181 @default.
• W2288573834 cites W2098836821 @default.
• W2288573834 cites W2100336555 @default.
• W2288573834 cites W2106190040 @default.
• W2288573834 cites W2121847893 @default.
• W2288573834 cites W2124139886 @default.
• W2288573834 cites W2124177504 @default.
• W2288573834 cites W2126638392 @default.
• W2288573834 cites W2130858592 @default.
• W2288573834 cites W2135891781 @default.
• W2288573834 cites W2141759041 @default.
• W2288573834 cites W2143030437 @default.
• W2288573834 cites W2145188627 @default.
• W2288573834 cites W2151505523 @default.
• W2288573834 cites W2160202162 @default.
• W2288573834 cites W2167543058 @default.
• W2288573834 cites W2170884537 @default.
• W2288573834 cites W2171156871 @default.
• W2288573834 doi "https://doi.org/10.1016/j.jhep.2015.12.017" @default.
• W2288573834 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4822535" @default.
• W2288573834 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26743076" @default.
• W2288573834 hasPublicationYear "2016" @default.
• W2288573834 type Work @default.
• W2288573834 sameAs 2288573834 @default.
• W2288573834 citedByCount "159" @default.
• W2288573834 countsByYear W22885738342016 @default.
• W2288573834 countsByYear W22885738342017 @default.
• W2288573834 countsByYear W22885738342018 @default.
• W2288573834 countsByYear W22885738342019 @default.
• W2288573834 countsByYear W22885738342020 @default.
• W2288573834 countsByYear W22885738342021 @default.
• W2288573834 countsByYear W22885738342022 @default.
• W2288573834 countsByYear W22885738342023 @default.
• W2288573834 crossrefType "journal-article" @default.
• W2288573834 hasAuthorship W2288573834A5001501626 @default.
• W2288573834 hasAuthorship W2288573834A5003824543 @default.
• W2288573834 hasAuthorship W2288573834A5003995610 @default.
• W2288573834 hasAuthorship W2288573834A5004309561 @default.
• W2288573834 hasAuthorship W2288573834A5005888483 @default.
• W2288573834 hasAuthorship W2288573834A5010503980 @default.
• W2288573834 hasAuthorship W2288573834A5019716566 @default.
• W2288573834 hasAuthorship W2288573834A5022140384 @default.

• next