The analysis identified a set of antibody species that occur more often in patients with ME/CFS and FM than in healthy controls. Through this analysis we aim to map antigens back to particular organisms in the environment that may give rise to these antibodies in some ME/CFS and FM patients.
This preliminary result was intriguing enough that the next batch of 150 blood samples was sent to Serimmune last week to confirm these results as well as expand the number of antigens that are recognized. We hope to publish these results in early 2019.
Cytokine signature associated with disease severity in chronic fatigue syndrome patients https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576836/ Although the inclusion of fatigue duration as an additional covariate was expected to result in a loss of statistical power, regression analysis by both disease severity and fatigue duration revealed that the upward linear trend across disease severity remained statistically significant for CCL11, CXCL10, G-CSF, GM-CSF, IFN-γ, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, LIF, NGF, ICAM1, and resistin. The findings by severity for CXCL1, SCF, and TGF-α shifted slightly above the threshold for statistical significance (CXCL1, adjusted P = 0.0536; SCF, adjusted P = 0.0531; TGF-α, adjusted P = 0.0797), possibly because of variance inflation (18) by the independent covariate of fatigue duration. Only CXCL9 and IL-1α inversely correlated with fatigue duration but lost statistical significance after correction for multiple comparisons (SI Appendix, Table S2).
Remarkably, 17 cytokines were associated with severity in ME/CFS patients. Thirteen of these 17 cytokines are primarily proinflammatory: CCL11, CXCL1, CXCL10, IFN-γ, IL-4, IL-5, IL-7, IL-12, IL-13, IL-17, leptin, G-CSF, and GM-CSF.
By picking CXCL10(for example):
CXCL10/IP-10 in Infectious Diseases Pathogenesis and Potential Therapeutic Implications https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203691/ Inflammation is associated with secretion of CXCL10 from leukocytes, neutrophils, eosinophils , monocytes, epithelia, endothelial and stromal cells, and keratinocytes in response to IFN-γ [2-3]. CXCL10 specifically activates CXCR3 receptor, a seven trans-membrane-spanning G protein-coupled receptor (GPCRs) , which is predominantly expressed on activated T, B lymphocyte , natural killer (NK), dendritic and macrophage cells. CXCL10 induces chemotaxis, apoptosis, cell growth inhibition and angiostasis. Abnormal levels of CXCL10 have been observed in body fluids of individuals infected with viruses [1, 6-7], bacteria [8-9], fungi  and parasites [11-13] indicating an important role in pathogenesis of these diseases.
A random-sequence peptide microarray can interrogate serum antibodies in a broad, unbiased fashion to generate disease-specific immunosignatures. This approach has been applied to cancer detection, diagnosis of infections, and interrogation of vaccine response. We hypothesized that there is an immunosignature specific to ME/CFS and that this could aid in the diagnosis. We studied two subject groups meeting the Canadian Consensus Definition of ME/CFS. ME/CFS (n?=?25) and matched control (n?=?25) sera were obtained from a Canadian study. ME/CFS (n?=?25) sera were obtained from phase 1/2 Norwegian trials (NCT01156909). Sera from six healthy controls from the USA were included in the analysis. Canadian cases and controls were tested for a disease immunosignature. By combining results from unsupervised and supervised analyses, a candidate immunosignature with 654 peptides was able to differentiate ME/CFS from controls. The immunosignature was tested and further refined using the Norwegian and USA samples. This resulted in a 256-peptide immunosignature with the ability to separate ME/CFS cases from controls in the international data sets. We were able to identify a 256-peptide signature that separates ME/CFS samples from healthy controls, suggesting that the hit-and-run hypothesis of immune dysfunction merits further investigation. By extending testing of both our signature and one previously reported in the literature to larger cohorts, and further interrogating the specific peptides we and others have identified, we may deepen our understanding of the origins of ME/CFS and work towards a clinically meaningful diagnostic biomarker.
I visited the BHC about 2 months ago and asked Suzanne about this. She was very excited about it. She said it was using new technology. She tried to get together an antibody study using researchers across the country at least 5 years ago - well before the recent interest in autoimmunity. It seemed very promising given the people she got interested in it - many of whom I'd never heard of - but the grant was denied.
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