Review of the potential value of serum interleukin levels as prognostic biomarkers of liver failure

Figure 2 Molecular mechanisms underlying the involvement of interleukin 21 (IL-21), IL-22, and IL-31 in liver failure (diagram depicts the signaling pathway of ILs and their involvement in liver failure). It starts with a CD4+ T cell or immune cell at the top, which secretes three different types of interleukin (IL): IL-21, IL-22, and IL-31. Each IL binds to its specific receptor on the cell surface: IL-21 binds to the IL-21 receptor (IL-21R), IL-22 binds to the IL-10R2 and IL-22R1, and IL-31 binds to the IL-31RA and oncostatin M receptor (OSMR). These receptors activate downstream signaling pathways involving Janus kinase 1 (JAK1), JAK2, JAK3, and tyrosine kinase 2 (TYK2), which phosphorylate signal transducer and activator of transcription (STAT) proteins. The activated STAT proteins then translocate to the nucleus and regulate gene expression, activating phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) signaling pathways. The diagram shows that these signaling events ultimately lead to liver failure through various mechanisms, including increased levels of liver enzymes (alanine aminotransferase [ALT], aspartate aminotransferase [AST], total bilirubin [TBIL], alpha-fetoprotein [AFP], model for end-stage liver disease [MELD]), liver cirrhosis, hepatitis B, and liver fibrosis, which highlights the complex interplay between immune cells, ILs, and signaling pathways in the pathogenesis of liver failure.) APAP: Acetaminophen; CCl4: Carbon tetrachloride; ConA: Concanavalin A; LPS: Lipopolysaccharides.