Abstract
Distinct metabolic pathways are known to regulate growth, differentiation, survival, and activation of immune cells by providing energy and specific biosynthetic precursors. Compelling experimental evidence demonstrates that effector T cell functions are coupled with profound changes in cellular metabolism. Importantly, the effector T cell-dependent “anti-self” response characterizing the autoimmune diseases is accompanied by significant metabolic alterations. MicroRNAs (miRNAs), evolutionary conserved small non-coding RNA molecules that affect gene expression by binding to target messenger RNAs, are now known to regulate multiple functions of effector T cells, including the strength of their activation, thus contributing to immune homeostasis. In this review, we will examine the most recent studies that describe miRNA direct involvement in the metabolic reprogramming that marks effector T cell functions. In particular, we will focus on the work showing a connection between miRNA regulatory function and the molecular network dysregulation that leads to metabolic pathway derangement in autoimmunity. Finally, we will also speculate on the possibility that the interplay between miRNAs and metabolism in T cells may help identify novel miRNA-based therapeutic strategies to treat effector T cell immunometabolic alterations in pathological conditions such as autoimmunity and chronic inflammation.
Highlights
The immune system encompasses a variety of cellular subsets that are highly dynamic and specialized in several activities essential for host defense and tissue homeostasis [1,2,3,4]
It has been recently reported that miR-633 that targets the AKT/mammalian target of rapamycin (mTOR) pathway is significantly reduced in CD4+ T cells from systemic lupus erythematosus (SLE)-affected subjects, and its expression negatively correlates with disease activity [Table 1; [135]]
These results suggest an important role for miR-99 family, in particular the miR-99b-5p, in T cell activation during multiple sclerosis (MS) through a hyper-activation of the mTOR pathway in pathogenic lymphocytes
Summary
Distinct metabolic pathways are known to regulate growth, differentiation, survival, and activation of immune cells by providing energy and specific biosynthetic precursors. Compelling experimental evidence demonstrates that effector T cell functions are coupled with profound changes in cellular metabolism. The effector T cell-dependent “anti-self” response characterizing the autoimmune diseases is accompanied by significant metabolic alterations. MicroRNAs (miRNAs), evolutionary conserved small non-coding RNA molecules that affect gene expression by binding to target messenger RNAs, are known to regulate multiple functions of effector T cells, including the strength of their activation, contributing to immune homeostasis. We will examine the most recent studies that describe miRNA direct involvement in the metabolic reprogramming that marks effector T cell functions.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.