Abstract # 3191 From biomarkers to targeted treatment: The myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and gulf war illness (GWI) story
Publication date: February 2019Source: Brain, Behavior, and Immunity, Volume 76, SupplementAuthor(s): N.G. Klimas, M.A. Fletcher, M.M. Abreu, K. Aenlle, T. Craddock, G. BroderickA model of pathogenesis of ME/CFS and GWI includes genetic predisposition and presence of a triggering event such as exposure (GWI) or infection (ME/CFS). Important mediators of disease include autonomic, endocrine, neuroendocrine, sleep, psychosocial, immune, viral reactivation or persistence, as well as other antigenic exposures (e.g. microbiome). We’ve found immune abnormalities in ME/CFS which consist of several types of immune activation with an increase in expression of DR, CD26, CD38; a shift to TH2 cytokines with pro-inflammatory cytokine expression of TNF-alpha, IL-1, and IL-6 and increased NPY and sCD26 levels. There are functional defects in T and B cells and in vitro NK cell cytotoxicity is markedly decreased as are perforin and granzymes in both NK and CD8 phenotypes. Using a systems biology approach, research subjects are challenged with exercise, and the team maps out the cascade of events across immune, neuroendocrine, autonomic and bioenergenic domains to create a firm understanding of the underlying homeostatic networks. Taken together, we use a virtual platform that has predicted specific subgroups in ME/CFS and GWI to model illness and intervention. Running thousands of virtual trials in various combinations and time courses, the computational team have provided clinical trial de...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research
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