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Neuroinflammation in ME/CFS was initially suggested by studies showing elevated levels of pro-inflammatory cytokines, and decreased anti-inflammatory cytokines, in cerebrospinal fluid from lumbar punctures in ME/CFS patients [62, 63], and further supported by a positron emission tomography (PET) study [64], which showed increased binding of a radioligand to 18 kDa translocator protein (TSPO) receptor, the expression of which increases when microglia are activated

Accumulated evidence suggests that ROS function as second messengers in the determination of cell fate and the modification of various signaling molecules [41]

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