Cell Res . . . Chi Hongbo team publishes the latest signal networks in immune metabolism (worth collecting)

Inature adaptive immunity is essential for the eradication of pathogens and tumors, but it may also cause uncontrolled or pathological inflammation.T cell receptor, costimulatory signal and cytokine signal jointly determine the specific signal network that triggers T cell activation and functional programming.in addition, cellular metabolism promotes T cell responses and is dynamically regulated by the interaction of serine / threonine kinases, immunological cues, and nutritional signaling networks.on March 20, 2020, Chi Hongbo team of St Jude Children's research hospital in Memphis, Tennessee, USA, published an online publication entitled "signaling networks in" on cell research This review summarizes the upstream regulatory proteins and signal transduction effectors of key serine / threonine kinase mediated signal transduction network, including PI3K – AGC kinase, mTOR and LKB1 – AMPK pathways, which regulate metabolism, especially in T cells.this review also provides a view on the outstanding issues and clinical applicability of immunometabolic signals.understanding the regulatory proteins and effectors of immune metabolic signaling networks may reveal therapeutic targets to regulate metabolic processes and T-cell responses in human diseases.the adaptive immune system is composed of T cells and B cells, which is essential for host response to invasive pathogens and tumors.in the presence of costimulatory and cytokine signals, once the T cell receptor (TCR) recognizes the relevant antigen, it will activate the signal network in immature T cells to promote clonal expansion, effector cell differentiation and immune function.after antigen elimination, most effector cells will die due to programmed cell death, but some cells will exist for a long time like memory cells and prepare for rapid recall reaction.the activation state and subsets of T cells indicate obvious cellular heterogeneity.the role of PI3K – AGC signal transduction in T cell activation and metabolic reprogramming has been recognized in recent years.static cells such as naive or memory T cells facilitate mitochondrial driven catabolism, including oxidative phosphorylation (OXPHOS).after activation, T cells undergo static withdrawal partially catalyzed by nutrients such as glucose and glutamine.is used to generate enough macromolecules for cell growth and support the increased energy demand associated with this growth.this metabolic reprogramming not only includes the increase of aerobic glycolysis and glutamine decomposition, but also the significant up regulation of mitochondrial biogenesis and function.in addition, these changes in the metabolic program must be appropriately regulated to maintain immune homeostasis and functional specificity of T cell subsets.therefore, how to regulate the metabolic process through upstream signal network and rewire the role of metabolism in T cells is still the key to solve the problem. metabolic programming in T cells through LKB1 and AMPK signaling. In this review, the cellular signaling pathways involved in immunometabolic regulation, including related molecules, upstream and downstream targets and their cell type specific effects, are discussed. specifically, the discussion focused on phosphoinositide 3 kinase (PI3K) - protein kinase A, G and C (AGC) kinases, target of rapamycin (mTOR) and lkb1-5'amp activated protein kinase (lkb1-ampk) signal. in addition, the paper also reviews the emerging research interests in these approaches and the potential areas for future research. therefore, this review provides the necessary information about molecular signal transduction, especially the background research on immune metabolism in T cells, and emphasizes how this field can promote the development of human disease treatment. reference message: