Lower frequency of IL-17F sequence variant (His161Arg) in chronic fatigue syndrome patients.

Abstract: Chronic fatigue syndrome (CFS) is characterized by immune dysfunctions including chronic immune activation, inflammation, and alteration of cytokine profiles. T helper 17 (Th17) cells belong to a recently identified subset of T helper cells, with crucial regulatory function in inflammatory and autoimmune processes. Th17 cells are implicated in allergic inflammation, intestinal diseases, central nervous system inflammation, disorders that may all contribute to the pathophysiology of CFS. IL-17F is one of the pro-inflammatory cytokines secreted by Th17 cells. We investigated the association between CFS and the frequency of rs763780, a C/T genetic polymorphism leading to His161Arg substitution in the IL-17F protein. The His161Arg variant (C allele) antagonizes the pro-inflammatory effects of the wild-type IL-17F. A significantly lower frequency of the C allele was observed in the CFS population, suggesting that the His161Arg variant may confer protection against the disease. These results suggest a role of Th17 cells in the pathogenesis of CFS.

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Non-invasive structural and functional neuroimaging in ME/CFS - Prof. Basant Puri.

Aims: ME/CFS is a condition characterised by persistent mental and physical fatigue accompanied by a range of neurological, autonomic, neuroendocrine, immune and sleep difficulties (Carruthers et al, 2003). Recent functional neuroimaging techniques (Lange et al, 2005) have illustrated an increased neural resource allocation in participants with ME/CFS when completing complex auditory tasks. In regard to brain biochemistry, three recent research studies (two systematic studies: Puri et al, 2002 and Chaudhuri et al, 2003; and one case series: Tomoda et al, 2000) employing magnetic resonance spectroscopy have shown that there are changes in the chemistry of the brain in patients with ME/CFS. Each of these three studies has shown a significant increase in cerebral choline levels, a result that is consistent with an impairment in the biosynthesis of membrane phospholipids or an increased breakdown of these molecules (Puri, 2005).

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An Investigation into Biochemical and Blood Flow Aspects of ME/CFS in Children

The aim of this investigation is to examine whether biochemical abnormalities similar to those already observed in adults with ME/CFS also exist in a group of children with the illness (in whom there is the possibility of long-lasting chronic ill-health).
The study will be based at the Vascular Diseases Research Unit, University of Dundee, which in the past 15 years has published more than 250 peer-reviewed scientific papers relating to inflammation and vascular disease, and over the past 4 years has been investigating ME/CFS in adults. The study on children is an extension of this work on adults, and fits in well with the UK Chief Medical Officer’s call in 2002 for further research in this field.

Dr. Jonathan Kerr's work

Dr Jonathan Kerr of Imperial College London, supported by the CFSRF, published a paper containing early results in the Journal of Clinical Pathology (J Clin Path 2005; 8:860-863, pdf format) in August 2005.

Fifteen genes were discovered to be up to 4 times as active in ME sufferers compared with a control group. Dr. Kerr is continuing his studies using a larger group of patients.

A gene expression profile investigation is being carried out by another team at the Centres for Disease Control and Prevention's in Atlanta (see From Scepticism to Science). Preliminary findings of these groups suggest dysregulation of genes involved in immune pathways which lend support to the evidence of immune dysregulation in the pathogenesis of ME/CFS  (thanks to MERGE for sourcing this news).