Published online Jun 28, 2019. doi: 10.5500/wjt.v9.i2.27
Peer-review started: September 12, 2018
First decision: October 5, 2018
Revised: October 25, 2018
Accepted: January 28, 2019
Article in press: January 28, 2019
Published online: June 28, 2019
Processing time: 289 Days and 9 Hours
Organ transplantation is a life-saving procedure, however predicting graft survival is still challenging. Understanding immune-cell pathobiology is critical to the development of effective therapies to prevent rejection. Over the recent years it has become progressively evident that the complex nature of immune cell behavioral dynamics is strongly dependent on cellular metabolism, which in turn, relies on competition for nutrients, oxygen and metabolites with other immune cells and microbiota. Furthermore, the influence of the inflammatory state can lead to substantial changes in conditions within the tissue micro-environment. Considering the context of immunity, alterations in metabolic pathways (glycolysis, the tricarboxylic acid cycle, the pentose phosphate pathway, the fatty acid oxidation and synthesis, and the amino acid metabolic pathways) will influence the production of different sets of cytokines and affect transplantation outcome. It is now known that naïve, resting and effector cells acquire different metabolic profiles and studies have shown that specifically targeting some of these metabolic routes can prevent differentiation of effector T cells in favor of Tregs. Ultimately, to develop effective therapies that will prevent graft loss and understanding how cell metabolism impacts the fate and function of immune cells is now a critical point of discussion. The distinct metabolic features and requirements observed in effector and suppressive cell subsets offer promising opportunities for selective regulation of the immune responses in transplantation and will be discussed in this review.
Core tip: In this review we summarize the most recent findings on metabolic pathways involved in the determination of immune cell fate and highlight the relevance of understanding how metabolic reprogramming is involved in the activation of dendritic cells and T cells, as well as development of strategies that target metabolic reprogramming to counteract effector cell activation in order to prevent graft failure.