Two new studies looking at intracellular immune dysfunction in chronic fatigue syndrome suggest a link with symptoms and provide targets for new treatments.

Chronic fatigue syndrome (CFS) is a serious chronic illness which continues to baffle doctors and researchers and leaves those with the condition frustrated and despairing.

Although dismissed as something akin to hypochondria or attention seeking by much of the medical profession for many years it has been clear since the very first biochemical studies into CFS that immune dysfunction was a large component of the illness.

Many people seem to develop CFS after viral infections which don't seem to clear up properly. Patients continue to suffer with flu-like symptoms such as sore throats, enlarged/sore glands, and problems with temperature control. This all suggests that the immune response to the original infection is not switched off as it should be once the virus has been defeated. This has led researchers to look at various markers of ongoing immune system activation in CFS patients.

In a recent paper researchers from the University of Brussels, Belgium report that evidence demonstrating intracellular immune dysfunctions in CFS patients is accumulating. They note however that this has not been adequately investigated as a therapeutic target.

The researchers conducted a thorough review of all published scientific literature relating to intracellular immune dysfunction in CFS and sought to find connections between this and other confirmed immune abnormalities such as deficiency of naturak killer (NK) cells, as well as symptoms such as fatigue and poor exercise tolerance. The hope being that this would point the way to the development of future treatments.

The primary finding of the review was that in CFS patients there are consistent abnormalities in an enzyme known as RNase L which is vital for proper intracellular immune function. These abnormalities include increases in both the production and breakdown of RNase L. This enzyme is receiving much interest in CFS researh circles as researchers try to home in on key dysfunctions in the conditions. The Belgian researchers conclude that based on the available evidence RNase L pathways are a promising target for future CFS therapies.

They also found an increased rate of immune cell apoptosis (programmed cell death) in CFS patients.

Meanwhile, a larger team of researchers at the University of Belgium (including those involved with above review), conducted a study involving 16 CFS patients to determine if immune abnormalities correlated with the patients' symptoms. Again, RNase L was a major target for the research along with related biochemical markers elastase and protein kinase R (PKR).

Each of the patients was asked to complete questionnaires relating to their ability to perform daily activities and then had blood samples taken to measure various immune system parameters.

After analysing the results the team found that increased elastase activity and the resultant increase in RNase L cleavage was accompanied by increased activity of both the RNase L and PKR enzymes. They conclude that RNase L and elastase activity are linked to the level of debility in CFS patients and that these immune abnormalities are therfore clinically significant.

What this work from the University of Belgium demonstrates is that these immune system abnormailities are central to the illness and targetting treatment at correcting the dysfunction is likely to bring improvements in the symptoms experienced by CFS patients. It may well be that this intracellular immune dysfunction is the root cause of the disease process so effective treatment of this may one day produce a cure.

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