USA: Center for Solutions for ME/CFS - news and updates from Columbia University's NIH funded center

Dakota15 said:
From the report: “Earlier this month, Ian Lipkin, M.D., and his team at Columbia University submitted a paper for publication that suggests certain approved drugs could possibly be repurposed…”
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I wonder on what basis? I don't remember him coming up with any findings, let alone anything that would point to particular drugs, but maybe I just haven't been following the work closely enough.
 
I guess I’m saying I like it when researchers explicitly state which specific drugs they recommend for trials (even if they end up being wrong). In most of these papers I see a lot of handwaving or very vague recommendations like “anti-inflammatories”, etc.
 
forestglip said:
Can you say a bit more about why it might be useful?
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IL-17 is a T cell derived cytokine that probably does lots of things. It seems to be involved in seronegative spondarthropathies which for me are the closest analogy I can think for what might be going on in ME/CF immunology. I don't have any more specific justification than that but at least it is about as logical as using rituximab if you think antibodies cells are involved.

I mentioned it Lipkin because he has given a presentation that mentioned IL-17 levels in ME/CFS. I seem to remember that Mady Hornig found a difference. I think the justification was moot but I would probably put it ahead of a lot of other things. IL-17 blockers have been used in other conditions and seem fairly safe.
 
Jonathan Edwards said:
Funny you should say that.
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What are the chances of the non-biologists among us understanding your paper? Wondering if you could maybe write a very top-level summary of the key ideas that ordinary PwME could understand that S4ME or others could put out on social media, especially as it's likely that your paper will get a lot of attention, particularly once you put it up on Queios.

It would be better if you could provide a lay summary rather than random people making a hash of it and circulating a duff version.

Very excited about this paper! Can't wait!
 
Reposting @Dakota15 post on USA news thread. This may be a chance for folks to ask questions they have about Ian Lipkin's teams research. Takes place 6pm UK time on 9th April 2025.
Dakota15 said:
Boosting from #NotJustFatigue.

https://twitter.com/user/status/1909671972327276879


Text: "Just received word that Dr. W. Ian Lipkin is doing a live podcast with Howard Zucker TOMORROW Wednesday April 9 at 1 pm ET. It’s an opportunity for members of the community to ask questions and highlight concerns. LINK: https://letshang.live/event/d8f2e132-docology-world-health-alert "
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Jonathan Edwards said:
IL-17 is a T cell derived cytokine that probably does lots of things.
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A few papers from the last 6 months relating to IL-17 —

Brain-wide mapping of immune receptors uncovers a neuromodulatory role of IL-17E and the receptor IL-17RB (2025, Cell)
• IL-17 receptor subunits exhibit distinct neuronal expression patterns in the brain
• IL-17RB and its interaction with IL-17E in the S1DZ promote social behavior
• IL-17E functions as a neuromodulator in cortical neurons
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The Role of IL-17A in Mediating Inflammatory Responses and Progression of Neurodegenerative Diseases (2025, International Journal of Molecular Sciences)
Emerging evidence indicates its capacity to activate microglial cells and astrocytes, subsequently inducing the production of inflammatory mediators that exacerbate neuronal injury and functional impairment. Clinical observations have revealed a demonstrated association between IL-17A concentrations and blood–brain barrier (BBB) dysfunction, creating a pathological feedback loop that amplifies neuro-inflammatory responses.
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Alterations in Gut Microbiome Composition and Increased Inflammatory Markers in Post-COVID-19 Individuals (2025, Molecular Neurobiology)
Noteworthy findings include a significant increase in the myeloid progenitor inhibitory factor 1 (MPIF-1), interleukin (IL)-17, and triglyceride among post-COVID-19 individuals.
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Rhythmic IL-17 production by γδ T cells maintains adipose de novo lipogenesis (2024, Nature)
This study identifies a crucial role for IL-17 in whole-body metabolic homeostasis and shows that de novo lipogenesis is a major target of IL-17.
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Antinociceptive interactions between excitatory interferon-γ and interleukin-17 in sensory neurons (2024, Brain, Behavior, and Immunity)
We propose a novel form of inhibition in sensory neurons that allows the intrinsically excitatory IFNγ to attenuate pro-nociceptive effects of cytokines such as IL-17 through interactions with voltage-gated Na+ currents.
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Double negative T cells promote surgery-induced neuroinflammation, microglial engulfment and cognitive dysfunction via the IL-17/CEBPβ/C3 pathway in adult mice (2024, Brain, Behavior, and Immunity)
The results showed an increased hippocampus infiltration of DNTs with augmented IL-17 production, along with C3 upregulation and cognitive impairment. Both inhibition of IL-17 or knock-down of CEBPβ significantly suppressed C3 expression, synaptic engulfment by microglia and attenuated cognitive impairment.
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Stuart79 said:
Has this group done anything to move the needle in ME/CFS?
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They have published extensively for 25 years, had close ties with the CDC via Ian Lipkin to try and influence things, and I think Ian Lipkin advocated strongly for the need for NIH Research centers with sufficient funding. They were the first to establish a biospecimen repository / biobank which NIH has now taken over. The team was planning to try and replicate DecodeME findings in a US cohort.

This is from NIH Reporter - they had one of two NIH center grants that were renewed for 5 years in 2024 but that was stopped by the freeze on Columbia University research.
https://reporter.nih.gov/search/YFuWk8CcR0CFVRcwMz0FfQ/project-details/10878252

Project 1, Molecular Correlates of Symptom Severity in ME/CFS, leverages advances in technology to create a smart phone app to track the course of illness and correlate with biological manifestations.

Project 2, Genotypic Analysis in ME/CFS, builds on the UK-based Decode ME project, investments by the research advocacy organization Solve ME in identifying ME/CFS cases in the US, and the investments made in genotyping 400,000 control subjects in the Kaiser Permanente Research Bank (KPRB) to identify genotypic differences using Genome Wide Association Studies (GWAS) in the US.

Project 3, Pathogen Discovery through Longitudinal Serological Surveillance in ME/CFS, will search for evidence of exposure to infectious agents prior to and after ME/CFS diagnosis, using the unique resource of the Department of Defense Serum Repository and a new phage display method based on short peptides, that provides the granularity required to differentiate exposure to different viral agents as well as to differentiate acute, persistent, re-activated infections.

Ian Lipkin has publicly stated that they have some interesting work they need to finish up that they think can point to treatments.
 
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