Target Health Blog

Energy Changes in the Immune System in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

December 16, 2019


Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe, chronic, and debilitating disease that can cause a range of symptoms including pain, severe exhaustion, cognitive impairment, and post-exertional malaise, the worsening of symptoms after physical or mental activity. Estimates suggest that between 836,000 and 2.5 million people in the United States may be affected by ME/CFS. It is unknown what causes the disease and there are no treatments.  

New findings published in the Journal of Clinical Investigation (12 December 2019) suggest that specific immune T cells from people with ME/CFS show disruptions in the way they produce energy.

For the study, the authors examined biochemical reactions involved in energy production, or metabolism, in two specific types of immune cells obtained from 45 healthy controls and 53 people with ME/CFS. The authors focused on CD4 T cells, which alert other immune cells about invading pathogens, and CD8 T cells, which attack infected cells. The team used state-of-the-art methods to look at energy production by the mitochondria within T cells, when the cells were in a resting state and after they had been activated. Mitochondria are biological powerhouses and create most of the energy that drives cells.  

Results showed no significant differences in mitochondrial respiration, the cell's primary energy-producing method, between healthy and ME/CFS cells at rest or after activation. However, results suggest that glycolysis, a less efficient method of energy production, may be disrupted in ME/CFS. Compared to healthy cells, CD4 and CD8 cells from people with ME/CFS had decreased levels of glycolysis at rest. In addition, ME/CFS CD8 cells had lower levels of glycolysis after activation. The authors also looked at mitochondrial size and membrane potential, which can indicate the health of T cell mitochondria. CD4 cells from healthy controls and people with ME/CFS showed no significant differences in mitochondrial size nor function. However, CD8 cells from people with ME/CFS showed decreased membrane potential compared to healthy cells during both resting and activated states.

The authors than examined associations between cytokines, chemical messengers that send instructions from one cell to another, and T cell metabolism. The findings revealed different, and often opposite, patterns between healthy and ME/CFS cells, suggesting changes in the immune system. In addition, the presence of cytokines that cause inflammation unexpectedly correlated with decreased metabolism in T cells.

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