Ankylosing Spondylitis Research Reagents

Ankylosing spondylitis (AS), now classified under axial spondyloarthritis (axSpA), is a chronic inflammatory disease of the sacroiliac joints and spine with a strong HLA-B27 association (>90% of patients). The disease is driven by entheseal inflammation, where tissue-resident innate immune cells (ILC3, γδ T cells) produce IL-17A independently of classical Th17 differentiation. A paradoxical feature of AS is the coexistence of inflammation with pathological new bone formation (syndesmophytes), leading to progressive spinal ankylosis. Treatment includes NSAIDs, anti-TNF-α (adalimumab, infliximab, etanercept), anti-IL-17A (secukinumab, ixekizumab), and JAK inhibitors (tofacitinib, upadacitinib).

Research Use Only (RUO)Not intended for diagnostic or therapeutic procedures.

Ankylosing Spondylitis Research Reagents — key pathogenic pathways including HLA-B27, IL-17A entheseal inflammation, TNF-alpha, and pathological new bone formation

Fig. 1 Key pathogenic pathways and research targets in ankylosing spondylitis. HLA-B27 misfolding and homodimer formation; IL-17A from entheseal innate immune cells; TNF-α-driven sacroiliac inflammation; pathological new bone formation via BMP/Wnt signaling. Key research targets highlighted in orange.

abinScience provides validated anti-HLA-B27 recombinant antibodies with fluorescent conjugates for flow cytometric typing, anti-IL-17A reference antibodies with ADA ELISA kits for secukinumab and ixekizumab, and anti-TNF-α ADA toolkits for adalimumab and infliximab monitoring. All products are manufactured by our parent company AtaGenix Laboratories under ISO quality systems. Browse products below or contact us for custom antibody development.

Key Research Targets

HLA-B27 — HLA-B27 is the strongest genetic risk factor for ankylosing spondylitis, present in >90% of AS patients. HLA-B27 misfolding in the endoplasmic reticulum triggers the unfolded protein response (UPR) and IL-23 production; free heavy chain homodimers on the cell surface activate NK and innate immune cells. Anti-HLA-B*27 recombinant antibody (clone H4H2) with fluorescent conjugates (FITC, PE, APC, PerCP) supports flow cytometric HLA-B27 typing, homodimer detection, and UPR/misfolding research.
→ Browse HLA-B27 antibodies

IL-17A — IL-17A is the central effector cytokine in AS, produced by entheseal-resident ILC3 and γδ T cells rather than classical Th17 cells. Anti-IL-17A biologics (secukinumab, ixekizumab) have demonstrated significant efficacy in AS clinical trials. abinScience offers ADA toolkits for both: reference antibodies, drug-level ELISA kits, anti-drug antibodies (neutralizing and non-neutralizing clones), and neutralizing antibody ELISA kits for immunogenicity monitoring.
→ Browse IL-17A antibodies, proteins & ELISA kits

TNF-α — TNF-α drives sacroiliac and spinal inflammation and remains the most widely used biologic target in AS. Anti-TNF-α agents (adalimumab, infliximab, etanercept, golimumab, certolizumab) are recommended as first-line biologics for active AS failing NSAIDs. abinScience offers complete ADA toolkits for adalimumab and infliximab: reference antibodies, drug-level ELISA, ADA ELISA, and neutralizing antibody ELISA kits for TDM research and biosimilar development.
→ Browse TNF-α antibodies, proteins & ELISA kits

IL-23 (p19) — The IL-23/IL-17 axis is the central pathogenic pathway in AS, with IL-23 driving innate immune cell activation at entheseal sites. Although anti-IL-23 p19 monotherapy has shown mixed results in AS clinical trials (unlike its success in psoriasis), IL-23 remains a critical upstream research target for understanding the divergent biology of entheseal vs dermal IL-17 production. Anti-IL-23 p19 reference antibodies (guselkumab, risankizumab, tildrakizumab, mirikizumab, brazikumab) are available for pathway dissection studies.
→ Browse IL-23 antibodies, proteins & ELISA kits

References

1. Sieper J, et al. Axial spondyloarthritis. Lancet. 2017;390(10089):73-84. DOI

2. Baeten D, et al. Secukinumab, an interleukin-17A inhibitor, in ankylosing spondylitis. N Engl J Med. 2015;373(26):2534-2548. DOI

3. Deodhar A, et al. Upadacitinib for the treatment of active non-radiographic axial spondyloarthritis. Lancet. 2022;400(10349):369-379. DOI