Immune cell metabolism in autoimmunity

Abstract

Immune metabolism is a rapidly moving field. While most of the research has been conducted to define the metabolism of healthy immune cells in the mouse, it is recognized that the overactive immune system that drives autoimmune diseases presents metabolic abnormalities that provide therapeutic opportunities, as well as a means to understand the fundamental mechanisms of autoimmune activation more clearly. Here, we review recent publications that have reported how the major metabolic pathways are affected in autoimmune diseases, with a focus on rheumatic diseases.

Keywords: B cell; T cells; autoimmunity; systemic lupus erythematosus.

Figure 1

Metabolic mechanisms of T cell and dendritic cell activation and differentiation in autoimmunity. Glycolysis, glutaminolysis and lipid metabolism, as well as mammalian target of rapamycin (mTOR) activation and mitochondrial dysfunctions, have been shown to contribute to altered phenotypes in autoimmune T cells. Cholesterol synthesis and efflux contribute to altered phenotypes of autoimmune dendritic cells.

Figure 2

Metabolic mechanisms of B cell activation and differentiation in lupus. The integration of Toll‐like receptor (TLR)‐9 activation, type 1 interferon (IFN) signaling, mitochondrial metabolism and glycolysis determine the effector state of B cells in lupus.