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Cirrhosis-downregulated LSECtin can be retrieved by cytokines, shifts the TLR-induced LSECs secretome and correlates with the hepatic Th response.

Sebastian Martinez-LopezEnrique Ángel-GomisIsabel Gómez-HurtadoAnabel Fernández-IglesiasJavier MoranteJordi Gracia-SanchoPaula BoixFrancisco Javier CuberoPedro ZapaterEsther CaparrósRubén Frances
Published in: Liver international : official journal of the International Association for the Study of the Liver (2024)
LSECtin restrains TLR proinflammatory secretome induced on LSECs by interfering immune response control, survival and MAPKs signalling pathways. The cytokine-dependent induction of LSECtin and the association between LSECtin loss and Th17 cell subset expansion in the liver, provides a solid background for exploring LSECtin retrieval as a mechanism to reprogram LSEC homeostatic function hampered during cirrhosis.
Keyphrases
  • immune response
  • toll like receptor
  • high glucose
  • diabetic rats
  • inflammatory response
  • single cell
  • drug induced
  • dendritic cells
  • nuclear factor
  • endothelial cells
  • bone marrow
  • free survival