Aberrations in the IO&NS pathways in ME/CFS | Reference(s) |
---|---|
Increased production of key inflammatory mediators, such as NFκB, COX-2, iNOS | |
Increased levels of proinflammatory cytokines | Fletcher et al. [12] |
Immune activation, with increased in vivo expression of activation markers, such as CD38, and Th 1-like or Th 2-like responses | Klimas et al. [13] |
Immunosuppression, for example, diminished natural killer cell activity (NKCA), and decreased ex vivo expression of activation markers, such as CD69 | |
Depleted antioxidant levels | Maes et al. [15] |
Increased levels of radical oxygen (ROS) and nitrogen species (RNS) | Kennedy et al. [16] |
Oxidative damage to membrane fatty acids, mitochondria, functional proteins and DNA | |
Autoimmune responses against oxidatively modified fatty acids and nitrated proteins (neoepitopes) | Maes et al. [9] |
Autoimmune reactions | Maes (review) [19] |
Gut dysbiosis and gut-derived inflammation with increased bacterial translocation | |
Mitochondrial dysfunctions with lower carnitine and coenzyme Q10 levels | Myhill et al. [24], Plioplys and Plioplys [25], Maes et al. [7] |
Upregulation and dysregulation of the 2'-5' oligoadenylate synthetase/RNase L pathway | Nijs and De Meirleir [26] |
Apoptosis pathways | |
Ion channel dysfunction (channelopathy) | Broderick et al. [29] |
Lowered omega-3 polyunsaturated fatty acids | Maes et al. [30] |