DrRob
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DrRob
@paddler44.bsky.social
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pmc.ncbi.nlm.nih.gov/articles/PMC...
A comprehensive analysis and resource to use CRISPR-Cas13 for broad-spectrum targeting of RNA viruses
The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and variants has led to significant mortality. We recently reported that an RNA-...
pmc.ncbi.nlm.nih.gov
May 14, 2025 at 7:21 PM
Reposted by DrRob
erictopol.bsky.social
The Master Disrupter for American Healthcare
erictopol.substack.com/p/mark-cuban...
@mcuban.bsky.social's @costplusdrugsbot.bsky.social is just the start!
Our conversation in the new Ground Truths podcast
with full transcript and links
Mark Cuban: A Master Disrupter for American Healthcare
Low cost medications with total transparency was just the beginning
erictopol.substack.com
December 20, 2024 at 4:05 PM
paddler44.bsky.social
It would be interesting to examine EMR data to explore whether T cell exhaustion in MECFS patients leads to higher incidence of cancer diagnosis or higher susceptibility to certain infections.
tomkindlon.bsky.social Tom Kindlon @tomkindlon.bsky.social · Dec 2
New US research:
Transcriptional reprogramming primes CD8+ T cells toward exhaustion in #MyalgicEncephalomyelitis / #ChronicFatigueSyndrome

www.pnas.org/doi/epub/10....

"these data identify T cell exhaustion as a component of ME"

#MEcfs #CFS #PwME
Significance Myalgic encephalomyelitis/chronic fatigue syndrome (ME) is a serious disabling chronic illness that lacks FDA-approved therapies. Comprehensive transcriptomic, epigenomic, and flow cytometric profiles of primary CD8+ T cell subsets implicate T cell exhaustion in pathophysiology. We show that T cells in ME cases are epigenetically predisposed toward terminal exhaustion & that exhaustion markers are upregulated following exercise challenge. Using single-cell genomics, we provide important information about the role of CD8+ T cell exhaustion development and progression. Our findings are consistent with the hypothesis chronic viral infection is a factor in ME; by dissecting the molecular basis of T cell dysfunction in ME, we offer potential avenues for treatment. Myalgic encephalomyelitis/chronic fatigue syndrome (ME) is a severe, debilitating disease, with substantial evidence pointing to immune dysregulation as a key contributor to pathophysiology. To characterize the gene regulatory state underlying T cell dysregulation in ME, we performed multiomic analysis across T cell subsets by integrating single-cell RNA-seq, RNA-seq, & ATAC-seq and further analyzed CD8+ T cell subpopulations following symptom provocation. Specific subsets of CD8+ T cells, as well as certain innate T cells, displayed the most pronounced dysregulation in ME. We observed upregulation of key transcription factors associated with T cell exhaustion in CD8+ T cell effector memory subsets, as well as an altered chromatin landscape and metabolic reprogramming consistent with an exhausted immune cell state. To validate these observations, we analyzed expression of exhaustion markers using flow cytometry, detecting a higher frequency of exhaustion-associated factors. Together, these data identify T cell exhaustion as a component of ME, a finding which may provide a basis for future therapies, such as checkpoint blockade, metabolic interventions, or drugs that target chronic viral infections.
December 4, 2024 at 3:46 PM