Breaking boundaries in ankylosing spondylitis: how innovative cell therapies reshape immunity
Ke · 2025 · Frontiers in Immunology
What this paper found
Reviews mesenchymal stem cell and CAR-T cell therapy approaches for AS. MSC therapy shifts inflammatory M1 macrophages toward anti-inflammatory M2; CAR-T is still experimental for AS specifically. Current treatments fail to improve long-term prognosis, cell therapy is positioned as the next frontier.
Why this is on the map
Where 'next-generation' AS therapy is heading. Pairs with Volarevic et al. on the broader autoimmune side.
On the map under these threads
DOI: 10.3389/fimmu.2025.1613502· 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.