Immmunometabolism of systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a potentially fatal chronic autoimmune disease which is underlain by complex dysfunction of the innate and adaptive immune systems. Although a series of well-defined genetic and environmental factors have been implicated in disease etiology, neither the development nor the persistence of SLE is well understood. Given that several disease susceptibility genes and environmental factors interact and influence inflammatory lineage specification through metabolism, the field of immunometabolism has become a forefront of cutting edge research. Along these lines, metabolic checkpoints of pathogenesis have been identified as targets of effective therapeutic interventions in mouse models and validated in clinical trials. Ongoing studies focus on mitochondrial oxidative stress, activation of the mechanistic target of rapamycin, calcium signaling, glucose utilization, tryptophan degradation, and metabolic cross-talk between gut microbiota and the host immune system.

Keywords: Adaptive immune system; Autoimmunity; Autophagy; Endosome traffic; Glucose; Glutathione; Immunometabolism; Innate immune system mitochondria; Kynurenine; Lysosome; Metabolism; Systemic lupus erythematosus; Tryptophan; mTOR.