More evidence that IL-11 drives cancer progression, this time by promoting CD8+ T cell exhaustion:
Also, there’s a number of epidemiological studies linking IL-6 to poorer cognitive function, as well as MR evidence that the relationship is causal. Would love to see an RCT looking at cognitive function when IL-6/11 is inhibited:
Unfortunately, none of the compounts on this list are likely to signifiantly inhibit IL-11 when ingested at reasonable concentrations in humans.
Some inhibition is better than none? Considering the inaccessibility of IL-11 inhibitors to the ordinary folks?
Yes I agree with that. My point is mainly that the odds of these interventions above having a significant inhibitory effect on IL-11 is low so taking them specially to inhibit IL-11 is most likely a waste of money. If someone takes them for some other purpose, then the small chance of a slight IL-11 inhibition would be like a potential added bonus.
I have been considering trying IL-6 Inhibitors or JAK Inhibitors, which is more readily available. I have severe eczema flare-ups at times, and my doctor is willing to prescribe JAK Inhibitors. Thoughts?
I started rapamycin for my psoriasis, which seems to be helpful and has a somewhat dose-dependent response. Most inflammatory skin diseases are immunotriggered.
I am also considering adding Doxycycline as some of you are doing.
1. Biologics (Monoclonal Antibodies): These large molecules directly target the IL-6 protein or its receptor.
2. Small Molecules (JAK Inhibitors): These oral medications block the downstream signaling activated by IL-6.
A new paper (open access):
The interleukin (IL)-1 pathway is a key mediator of inflammation and innate immune responses. Its dysregulation contributes to rheumatoid arthritis (RA) and autoinflammatory diseases (AIDs). In this study, we develop a recombinant adeno-associated virus (rAAV)-based gene therapy to deliver an inflammation-inducible, secreted human IL-1 receptor antagonist (sIL-1Ra) as a complementary approach to existing IL-1 blockers. rAAV-mediated expression of sIL-1Ra dampens IL-1 signaling and inflammatory arthritis in mice. As the expression of endogenous sIL-1Ra is tightly regulated by inflammation, we developed an rAAV vector that produces sIL-1Ra in response to pro-inflammatory cytokines and bone morphogenic proteins (BMPs) enriched in the inflamed joints of patients with RA. Remarkably, inflammation-inducible sIL-1Ra is more effective than constitutively expressed sIL-1Ra in ameliorating inflammatory arthritis in the mouse model of RA. These mice showed a significant reduction in circulating immune cells, expression of the genes associated with inflammatory responses, joint swelling, and bone destruction. Similar to patients with deficiency of IL-1Ra (DIRA), IL-1Ra-deficient mice spontaneously develop inflammatory arthritis and skeletal abnormalities, which are almost completely reversed by a single systemic administration of the sIL-1Ra-expressing rAAV vector. Collectively, our results highlight inflammation-inducible IL-1-targeted therapy using an rAAV vector as a long-lasting, pathophysiologic treatment for chronic inflammatory diseases.
https://www.cell.com/molecular-therapy-family/molecular-therapy/fulltext/S1525-0016(25)00736-1
I agree. I first started getting into supplements by reading Life Extension magazine and every article convinced me to buy something else. It was a complete waste of money.