Dysregulated Expression of Tumor Necrosis Factor in Chronic Fatigue Syndrome: Interrelations with Cellular Sources and Patterns of Soluble Immune Mediator Expression

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Abstract
Among a group of 70 individuals who met the criteria established by the Centers for Disease Control and Prevention (Atlanta) for chronic fatigue syndrome (CFS), 12%–28% had serum levels exceeding 95% of control values for tumor necrosis factor (TNF) α, TNF-β, interleukin (IL) 1α, IL-2, soluble IL-2 receptor (sIL-2R), or neopterin; overall, 60% of patients had elevated levels of one or more of the nine soluble immune mediators tested. Nevertheless, only the distributions for circulating levels of TNF-α and TNF-β differed significantly in the two populations. In patients with CFS—but not in controls—serum levels of TNF-α, IL-1α, IL-4, and sIL-2R correlated significantly with one another and (in the 10 cases analyzed) with relative amounts (as compared to β-globin or β-actin) of the only mRNAs detectable by reverse transcriptase-coupled polymerase chain reaction in peripheral-blood mononuclear cells: TNF-β, unspliced and spliced; IL-1β, lymphocyte fraction; and IL-6 (in order of appearance). These findings point to polycellular activation and may be relevant to the etiology and nosology of CFS.

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