While this is interesting, it seems that this theory doesn't fit the bill of IL-23/IL-17 activation. From reading your article, this exists in an IL-5/IL-13 axis. Not to mention, in AS, it is noted that EPC (eosinophilic progenitor cells) are depleted in AS patients (Link.) The drugs that would mitigate the effect you are talking about would be anti-eosinophilic in nature, as mentioned in the conclusion of your article (many drugs similar sounding to that of those that are prescribed for AS, however, they work on different interleukins.) The drug reslizumab is also listed to affect the same interleukin, and is indicated for asthma. I did have asthma growing up, so that is of some interest for me to ponder the lung association.

I think the loss of tolerance to self is causing inflammation that is degrading/depleting specific areas of the intestine of eosinophils, which is why they are found to be depleted in AS patients per the article above. Leaky gut is known to be associated with those that have joint/tendon and soft-tissue disorders. The inflammatory pathways activated by bacteria and other pathogens created by dietary carbs are the kind that can flag the immune system to produce TNF-alpha, which activates NF-kB signaling, which then promotes the IL-23/IL-17 axis. This is the axis described as being both a) correlated with changes in affected individuals through GWAS (genome-wide association studies) and b) the target of the other drugs people are taking (inhibiting their joint/tendon and bone. Rifaximin also works on NF-kB signaling, so the fact that it is beneficial for me and a few others reinforces that it is working on the same pathways as these other drugs, albeit a more targeted inhibition.

I have also been reading on how to stop HLA-B27's propensity to form homodimers, as those are the substances that are binding strange peptides and antigens. The HLA-B27 molecule folds slowly, which is what allows for the creation of homodimers. This activates the UPR (unfolded protein response,) in the cell, which upregulates both NF-kB and, subsequently, cytokine expression (the NF-kB upregulates TNFα, IL-1, IL-6, and IL-23. IL-23 is required for the survival of Th-17 cells.) It has also been shown that certain pathogens take advantage of this pathway, such as Salmonella. That particular pathogen utilizes the UPR to infect cells, and, in HLA-B27+ individuals, the bacterial load to the cell is quadrupled compared to controls! One approach is to reduce the formation of homodimers by using Sulfasalazine. I read into Sulfasalazine and the literature states that it is its IKB kinase inhibitory activity that reduces homodimer formation. These homodimers recognize natural killer cells (KIR3DL2) and these are present on the surface of Th17 cells, which release IL-17 when activated, who have been granted increased survival from the IL-23 via the upregulated UPR. (Link.)

So, I did some more digging on natural IKB kinase (both alpha and beta inhibitors.) Turns out, I was onto something with Baicalein, from skullcap. I mentioned I took it alongside Rifaximin with really great results. Turns out that Baicalein not only stimulates ~20 tight-junction proteins to help seal the leaky intestines, it's also an IKB kinase inhibitor (Link!)

The table provided in this study suggests that there are many natural substances that are IKB kinase inhibitors. Since baicalein is working well for me, I am willing to try a few other of these natural compounds to test their effects. The next goal would be to see how to regain dendritic cells in the intestines and to regain tolerance to self. This would effectively be a double-whammy. You'd reduce the UPR-induced stress as well as reduce the inflammation being upregulated in the intestinal cells.

P.S. I've also found this link between dendritic cells and HLA-B27. It seems that just like in so many of us who have had an "event," and then began to experience symptoms, the dendritic cells are activated after maturation. This starts a transient production of homodimers. These homodimers would then cause the associated binding of peptides and antigens, which then causes more stress. I believe this is why the disease takes time to build because these transient cycles occur over and over until the system is finally degraded enough from the constant barrage of inflammation due to these dendritic cells being activated (Link.)

Here, in continental Europe Rifaximin is prescribed for Crohne D.

I think what you are describing here is an inflammation of mesenteric lymph nodes where T cell–dependent IgA class switching takes place. However, in case of for example mine (during the first onsets of AAU and AS in general I performed Colonoscopy that indicated Eosinophilic Ileitis), it is more likely thateosinophils contribute to T cell–independent IgA class switching, which mainly occurs in the small intestinal lamina propria, where abundant numbers of eosinophils reside.
Notably the up regulation comes with caloric intake, that would explain the fact that in some instance prolonged fasting can bring benefits, at least for the poeple with similar to mine expressions (but how often we know what really is there, my colonoscopy was purely coincidental)

Eosinophilic link

What activates dendritic cells, and the mechanism could be explained above (interesting article).
Now I am thinking, due to different roots, paths AS was triggered, people fail biologics that answer to specific circumstances... bringing us back to the HLA B27 + predisposition as secondary phenomena in this vicious circle.

just food for thought not a challenge of any kind..., we are all in this