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Possible Causes: Immunology

It has been proposed that CFS may be caused by an immunologic dysfunction, for example inappropriate production of cytokines, such as interleukin-1, or altered capacity of certain immune functions.

One thing is certain at this juncture: there are no immune disorders in CFS patients on the scale traditionally associated with disease. Some investigators have observed anti-self antibodies and immune complexes in many CFS patients, both of which are hallmarks of autoimmune disease.

However, no associated tissue damage typical of autoimmune disease has been described in patients with CFS. The opportunistic infections or increased risk for cancer observed in persons with immunodeficiency diseases or in immunosuppressed individuals is also not observed in CFS.

Several investigators have reported lower numbers of natural killer cells or decreased natural killer cell activity among CFS patients compared with healthy controls, but others have found no differences between patients and controls. 

T-cell activation markers have also been reported to have differential expression in groups of CFS patients compared with controls, but again, not all investigators have consistently observed these differences.

One intriguing hypothesis is that various triggering events, such as stress or a viral infection, may lead to the chronic expression of cytokines and then to CFS. Administration of some cytokines in therapeutic doses is known to cause fatigue, but no characteristic pattern of chronic cytokine secretion has ever been identified in CFS patients.

In addition, some investigators have noted clinical improvement in patients with continued high levels of circulating cytokines; if a causal relationship exists between cytokines and CFS, it is likely to be complex.

Finally, several studies have shown that CFS patients are more likely to have a history of allergies than are healthy controls. Allergy could be one predisposing factor for CFS, but it cannot be the only one, since not all CFS patients have it.