Abnormalities of the immune system are frequently found in ME/CFS, and there is evidence that the “cytokine” transforming growth factor beta (TGF-b1), a protein molecule which regulates a wide variety of cell processes, might be involved. In fact, ME Research UK-funded work on ME/CFS at the University of Dundee found high concentrations of active TGF-b1 in addition to increased neutrophil apoptosis (an important process that controls infections and removes cells that have reached the end of their natural life), suggesting an association between TGF-b1 activity and abnormalities in immune cells.
Because of such evidence, researchers in Beijing funded by the National Natural Science Foundation of China investigated TGF-b1 production (mRNA expression) in white blood cells, which have a role in fighting infection. They recruited 63 ME/CFS patients, 50 healthy people, and 50 control subjects with other diseases such as liver or lung cancer, diabetes mellitus, systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, and primary Sjögren’s syndrome. They found that mean TGF-b1 mRNA expression was significantly higher in ME/CFS patients (1.17±0.58) than in disease controls (0.07±1.08) or healthy people (0.00±1.63), with no significant differences between disease controls and healthy controls.
Given that TGF-b1 is found in many tissues such as blood, brain and cerebrospinal fluid, and is heavily involved in the complex processes surrounding apoptotic programmed cell destruction, the authors suggest that the abnormally high levels – not found in the comparison group containing people with the range of other diseases – point to underlying disease processes in ME/CFS, such as a persistent or reactivating infection, or a toxic state indicated by accelerated apoptosis.
Reference: Up-regulation of TGF-β1 mRNA expression in peripheral blood mononuclear cells of patients with chronic fatigue syndrome. Zhang HY et al. J Formos Med Assoc 2011 Nov; 110(11): 701-4.