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Immunometabolism in Autoimmune Diseases Special Issue

The activation of immune cells and their differentiation in specialized effector subsets rely on specific cellular metabolic programs. It is therefore not surprising that a number of immunometabolic alterations have been reported in patients with autoimmune diseases, as well as in mouse models of these diseases. The metabolic programs that sustain the activation of healthy lymphocytes are reviewed by Bystrom et al. [1], which are contrasted with the metabolic programs that have been found in CD4+ T cells and B cells in autoimmune diseases, with a focus on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). These two rheumatic diseases share CD4+ T cells that are fueled by an over-activated mTOR signaling, but that differ by many other metabolic pathways, even when considering the same type of cells, such as Th17 cells. The specific metabolic phenotypes of CD4+ T cells were reviewed in detail comparatively between RA and in SLE by Wu et al. [2]. RA T cells shunt glucose away from glycolysis and energy building toward the pentose phosphate pathway (PPP) and cell-building biosynthesis, which leads to a hyper-reduced state. This defect, rooted in the miss-location of AM PK that limits is activation, increases T cell mobility and their ability to invade the inflamed joints. On the opposite, SLE T cells present an increased glycolysis and mitochondrial metabolism leading to oxidative stress. The molecular pathways that support metabolic defects in SLE T cells is further reviewed by Vukelic et al. [3]. In addition to increased glycolysis and mitochondrial oxidation, there is also evidence from mouse models that SLE T cells present an enhanced glutamine metabolism involved in the expansion of Th17 cells as well as follicular helper T (Tfh) cells, both of which being pathogenic in SLE. Finally, altered lipid metabolism related to lipid rafts and plasma membrane sphingolipids has been linked to the activation of SLE T cells. Mangal et al. provide an extensive review of the metabolic programs that support a broad array of immune cells, some of them with known alterations in RA, and others with potential defects that have not been investigated and may contribute to RA [4]. Building a detailed understanding of metabolic defects in autoimmune diseases, more specifically in RA and SLE T cells has leveraged the therapeutic potentials of metabolic targeting in these diseases. These translational potentials are reviewed by Piranavan et al. [5]. A number of experimental drugs targeting key metabolic enzymes or processes have shown efficacy in mouse models. The inhibition of mTOR with rapamycin Open Access