Experimental models of spondyloarthritis: Pathophysiological insights and translational challenges.
Morizot C · 2026 · Journal of autoimmunity
Reading the original? How to read a paper.
What this paper found
This review takes stock of the mouse and rat models used to study spondyloarthritis and what each has taught us: the gut-joint connection, IL-23-driven inflammation where tendons meet bone, and the TNF pathways that became today's drugs. No single model captures the whole disease, which is one reason lab findings so often fail to translate, and the authors map what better models would need.
Why this is on the map
A guide to how much weight to give the many animal studies on the map, and why some mechanisms seen in mice never reach patients.
On the map under these threads
DOI: 10.1016/j.jaut.2026.103607 · opens in a new tab. The full paper is on the publisher’s site, not here.
Related papers on the board
Papers sharing one or more threads with this one.
A disease-associated gene desert directs macrophage inflammation through ETS2
Nature
Identified a single 'switch' gene called ETS2, sitting on chromosome 21, that turns immune cells inflammatory across AS, IBD, and several other related diseases. Because no current drug targets ETS2, this points to a treatment direction beyond what's already available with TNF and IL-17 blockers.
HLA-B27-associated gut microbiota and amino acid perturbations promote ankylosing spondylitis through M1 macrophage activation
Gut Microbes
Shows that HLA-B27, the gene most strongly linked to AS, reshapes which bacteria live in the gut and how the body handles certain amino acids, which in turn activates the inflammatory immune cells driving the disease. Suggests targeting the gut and these metabolic changes could become a real treatment route.
Gut microbiota and ankylosing spondylitis: current insights and future challenges
Microbial Cell
Comprehensive review of how gut bacterial imbalance disrupts the IL-23/IL-17 inflammatory pathway and weakens the intestinal barrier in AS. Identifies the lack of standardised methodology and large cohorts as the bottleneck for translating this into treatments.
Dysbiosis of Gut Microbiota in Ankylosing Spondylitis Patients
Dove Medical Press
Confirms that intestinal dysfunction precedes or amplifies systemic inflammation in AS. Frames gut microbiota as the convergence point where genetic, immune, and microbial factors meet.