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Can the light of immunometabolism cut through “brain fog”?
Mady Hornig
Mady Hornig
Published February 10, 2020
Citation Information: J Clin Invest. 2020;130(3):1102-1105. https://doi.org/10.1172/JCI134985.
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Commentary

Can the light of immunometabolism cut through “brain fog”?

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Abstract

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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Mady Hornig

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