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Recent research published in the journal, Cell, has described how a novel type of fibroblast, called “scleroderma-associated fibroblasts” (ScAFs) are what drive systemic scleroderma.
Getting under the skin of an autoimmune disorder
Interestingly, minocycline (and all tetracyclines) are capable of immune-modulation in numerous ways, including its effects on “transforming growth factor” (known as TGF beta). These actions enable minocycline’s use, for instance in dentistry and ovarian cancer.
In SSc (and in other skin manifestations, such as discoid lupus) it seems there is a TGF-β-dependent pathway inducing fibrosis and that Minocycline may effectively act by modulating errant fibroblast activity associated with this process.
Why do you think it is the medical industry looks right past Tetracyclines when it comes to immuno-modulation?
Do you understand the entire process of SSc, and the pathways it takes? Do you know scientifically how Minocycline inhibits the process? I’ve been trying to understand it myself.
Hi SK;
For the last few years I have been saying that Interlukins and TGF 1B are the culprits in SD.I have a lot of info on this but it is too much to post here.If you want it send me a private message with your e mail address and I can send it to you.Hi SK,
I’m not a scientist, just a fellow patient, so my lay understanding of the extensive properties of tetracyclines to modulate immunity in SD is limited. SD research is, at best, thin on the ground and research like the above article just comes at a trickle. However, if you click the following link, in the Resources/Journal section of this website, you should find the articles posted informative in this regard:
Regarding your first question and why tetracyclines have been sidelined, you’ll find this info in the first few chapters of Henry Scammell’s book, The New Arthritis Breakthrough. Nothing much has changed since the book was published. What I always found intriguing is that as far back as the early part of the 20th century, rheumatic diseases were believed to be caused and driven by chronic, stealth infection. However, with the advent of cortisone and it’s miraculous properties to tamp down inflammation, mid-century, the field of rheumatology switched gears and began looking at ways to suppress immunity.
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