Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 130, Issue 3, Pages 1491-1505Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI132185
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Funding
- Simmaron Research
- National Institute of Allergy and Infectious Diseases (NIAID), NIH [R21AI117595]
- National Institute of Neurological Disorders and Stroke (NINDS), NIH [U54NS105541]
- NIH [1S10RR025502]
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease with no known cause or mechanism. There is an increasing appreciation for the role of immune and metabolic dysfunction in the disease. ME/CFS has historically presented in outbreaks, often has a flu-like onset, and results in inflammatory symptoms. Patients suffer from severe fatigue and postexertional malaise. There is little known about the metabolism of specific immune cells in patients with ME/CFS. To investigate immune metabolism in ME/CFS, we isolated CD4(+ )and CD8(+) T cells from 53 patients with ME/CFS and 45 healthy controls. We analyzed glycolysis and mitochondrial respiration in resting and activated T cells, along with markers related to cellular metabolism and plasma cytokines. We found that ME/CFS CD8(+) T cells had reduced mitochondrial membrane potential compared with those from healthy controls. Both CD4(+) and CD8(+) T cells from patients with ME/CFS had reduced glycolysis at rest, whereas CD8(+) T cells also had reduced glycolysis following activation. Patients with ME/CFS had significant correlations between measures of T cell metabolism and plasma cytokine abundance that differed from correlations seen in healthy control subjects. Our data indicate that patients have impaired T cell metabolism consistent with ongoing immune alterations in ME/CFS that may illuminate the mechanism behind this disease.
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