Dysregulated expression of soluble immune mediator receptors in a subset of patients with chronic fatigue syndrome: cross-sectional categorization of patients by immune status
ISBN or ISSN
Journal of Chronic Fatigue Syndrome
Publication Date / Copyright Date
Individuals with chronic fatigue syndrome (CFS) have significantly increased proportions of activated CD8+T cells, decreased natural killer (NK) cell cytotoxic and lymphoproliferative activities, elevated serum levels of tumor necrosis factor (TNF)-α and detectable TNF-β, interleukin (IL)-lβ, and IL-6 mRNA in peripheral blood mononuclear cells (PBMC). We report here that CFS patients as a group also have significantly higher levels, as compared to controls, of soluble TNF receptor type I (sTNF-RI or sCDl20a), sIL-6R (sCD126) and β2-microglobulin (β2-m), but not of IL-1 receptor antagonist (IL-1Ra). Correlative and population distribution studies that included lymphoid phenotypic distributions and function as well as soluble immune mediator expression levels revealed the existence of at least two mainly nonoverlapping immunological categories among CFS patients with either: (1) dysregulaled TNF-α/β expression in association with changes in the serum levels of IL-lα, IL-4, sIL-2R and IL-lRa, PBMC-associated expression of IL-1β, IL-6 and TNF-β mRNA, and T cell activation; or, (2) interrelated and dysregulated expression of sTNF-RI, sIL-6R, and β2-m and significantly decreased lymphoproliferative and NK cell cytotoxic activities. This preliminary systematization is of usefulness in the diagnosis, follow-up, and characterization of possible etiological agents for CFS.
Medical Specialties | Medicine and Health Sciences | Osteopathic Medicine and Osteopathy
Patarca, R.; Klimas, Nancy G.; Garcia, M. N.; Walters, M. J.; Dombroski, D.; Pons, H.; and Fletcher, Mary A., "Dysregulated expression of soluble immune mediator receptors in a subset of patients with chronic fatigue syndrome: cross-sectional categorization of patients by immune status" (1995). College of Osteopathic Medicine Faculty Articles. 466.