Navigating immune cell immunometabolism after liver transplantation. (April 2021)

• Record Type: Journal Article
• Authors: Zhang, Wenhui; Liu, Zhikun; Xu, Xiao
• Is Part Of: Critical reviews in oncology/hematology. Volume 160(2021)
• Publication Date: 2021-04
• Subjects: 2-DG 2-deoxy-d-glucose -- 3-PO 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one -- ACOD1 aconitate decarboxylase 1 -- α-KG α-ketoglutarate -- Akt protein kinase B -- AMPK adenosine 5'-monophosphate-activated protein kinase -- APC antigen-presenting cell -- Arg1 arginase 1 -- ATP adenosine triphosphate -- ATRA all-trans retinoic acid -- CAR chimeric antigen receptor -- CCL C-C motif ligand -- cDC conventional DC -- CTL cytotoxic T lymphocyte -- DC dendritic cell -- DON 6-diazo-5-oxo-l-norleucine -- ESRD end-stage renal disease -- ETC electron-transport chain -- FAO fatty acid oxidation -- Fas/FasL factor-associated suicide/factor-associated suicide ligand -- Flt3L FMS-like tyrosine kinase 3 ligand -- GALT gut-associated lymphoid tissue -- GVHD graft-versus-host disease -- HIF-1α hypoxia-inducible factor-1 alpha -- HLA human leukocyte antigen -- HSC hepatic stellate cell -- ICOS/ICOSL inducible costimulator/inducible costimulator ligand -- IDO indoleamine -- IFN-I type I interferon -- iNOS inducible nitric oxide synthase -- LPS lipopolysaccharide -- LT liver transplantation -- mDC myeloid DC -- MHC man histocompatibility complex -- mTOR/mTORC1 mammalian target of rapamycin/mammalian target of rapamycin complex 1 -- NK cell natural killer cell -- NLRP3 Nod-like receptor 3 -- NO nitric oxide -- OXPHOS oxidative phosphorylation -- PAMP pathogen associated molecular pattern -- PD-1/PD-L1 programmed cell death-1/programmed cell death-ligand 1 -- pDC plasmacytoid DC -- PGC-1α proliferator-activated receptor gamma coactivator-1 alpha -- PHD prolyl hydroxylase domain -- PI3K phosphatidylinositol 3-OH kinase -- PPAR peroxisome proliferator-activated receptor -- PPP pentose phosphate pathway -- PRR pattern recognition receptor -- RA retinoic acid -- Resv resveratrol -- ROS reactive oxygen species -- SDH succinate dehydrogenase -- STAT3 signal transducer and activator of transcription 3 -- TCA cycle tricarboxylic acid cycle -- TGF-β transforming growth factor beta -- TLR Toll-like receptor -- TNF-α tumor necrosis factor alpha -- Treg regulatory T cell; Immunometabolism -- Liver transplantation -- Immune cells -- Immune tolerance -- Metabolic reprogramming; Oncology -- Periodicals; Hematology -- Periodicals; 616.994
• DOI: 10.1016/j.critrevonc.2021.103227
• Languages: English
• ISSNs: 1040-8428

Abstract

Graphical abstract: Highlights: Metabolic programming ultimately affects immune cells activation status and their functional differentiation to further affect post-transplant complications. Targeting regulation signaling and metabolites induce immune tolerance by innate and adaptive immune cells. Targeting immunometabolism is a novel therapeutic approach to induce immune tolerance and prevent post-transplant complications after transplantation. Abstract: Liver transplantation (LT) is the most effective treatment for end-stage liver diseases. The immunometabolism microenvironment undergoes massive changes at the interface of immune functionalities and metabolic regulations after LT. These changes considerably modify post-transplant complications, and immune cells play an influential role in the hepatic immunometabolism microenvironment after LT. Therefore, adequate studies on the complex pathobiology of immune cells are critical to prevent post-transplant complications, and the interplay between cellular metabolism and immune function is evident. Furthermore, immune cells perform their specified functions, such as activation or differentiation, accompanied by alterations in metabolic pathways, such as metabolic reprogramming. This transformation remarkably affects post-transplant complications like rejection. By targeting different metabolic pathways, regulations of metabolism are employed to shape immune responses. These differences of metabolic pathways allow for selective regulation of immune responses to further develop effective therapies that prevent graft loss after LT. This review examines immune cells in the hepatic immunometabolism microenvironment after LT, summarizes possible mechanisms and potential prevention on rejection to acquire immune tolerance, and offers some insight into references for scientific research along with clinical treatment.