Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA.
Address correspondence to: Mady Hornig, Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, New York, New York 10032, USA. Phone: 212.342.9036; Email: email@example.com.
First published February 10, 2020 - More info
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a highly debilitating disease with heterogeneous constitutional and neurological complaints. Infection-like symptoms often herald disease onset, but no pathogen or immune defect has been conclusively linked. In this issue of the JCI, Mandarano et al. illuminate bioenergetic derangements of ME/CFS T cell subsets. CD4+ and CD8+ T cells had impaired resting glycolysis. CD8+ cells additionally showed activation-related metabolic remodeling deficits and decreased mitochondrial membrane potential; a subset had increased resting mitochondrial mass. Immune senescence and exhaustion paradigms offer only partial explanations. Hence, unique mechanisms of disrupted immunometabolism may underlie the complex neuroimmune dysfunction of ME/CFS.
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