garcia - you mentioned that LDN turns off Th17. The abstract below, which was posted on another thread, suggests that it's already turned off in ME.
Might this be a reason why LDN makes some of us worse?
Jenny
A Formal Analysis of Cytokine Networks in Chronic Fatigue Syndrome
Gordon Brodericknext terma, Corresponding Author Contact Information, E-mail The Corresponding Author, Jim Fuitea, Andrea Kreitza, Suzanne D Vernonb, Nancy Klimasc and Mary Ann Fletcherd
a Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
b The CFIDS Association of America, Charlotte, NC, USA
c Miami Veterans Affairs Medical Center, Miami, FL, USA
d Department of Medicine, University of Miami, Miami, FL, USA
Received 1 February 2010;
revised 21 April 2010;
accepted 28 April 2010.
Available online 4 May 2010.
Abstract
Chronic Fatigue Syndrome (CFS) is a complex illness affecting 4 million Americans for which no characteristic lesion has been identified. Instead of searching for a deficiency in any single marker, we propose that CFS is associated with a profound imbalance in the regulation of immune function forcing a departure from standard preprogrammed responses. To identify these imbalances we apply network analysis to the co-expression of 16 cytokines in CFS subjects and healthy controls. Concentrations of IL-1a, 1b, 2, 4, 5, 6, 8, 10, 12, 13, 15, 17 and 23, IFN-γ, lymphotoxin-α (LT-α) and TNF-α were measured in the plasma of 40 female CFS and 59 case-matched controls. Cytokine co-expression networks were constructed from the pair-wise mutual information (MI) patterns found within each subject group. These networks differed in topology significantly more than expected by chance with the CFS network being more hub-like in design. Analysis of local modularity isolated statistically distinct cytokine communities recognizable as pre-programmed immune functional components. These showed highly attenuated Th1 and Th17 immune responses in CFS. High Th2 marker expression but weak interaction patterns pointed to an established Th2 inflammatory milieu. Similarly, altered associations in CFS provided indirect evidence of diminished NK cell responsiveness to IL-12 and LTα stimulus. These observations are consistent with several processes active in latent viral infection and would not have been uncovered by assessing marker expression alone. Furthermore this analysis identifies key sub-networks such as IL-2:IFNγ:TNFα that might be targeted in restoring normal immune function.