Spondyloarthritis: Bridging autoimmunity and autoinflammation

Spondyloarthritis (SpA) represents a diverse group of immune-mediated inflammatory diseases, including ankylosing spondylitis, psoriatic arthritis, and reactive arthritis, uniquely positioned at the crossroads of autoimmunity and autoinflammation.

Unlike classical autoimmune diseases such as rheumatoid arthritis or purely autoinflammatory disorders, SpA embodies both adaptive and innate immune system dysregulation.

Key pathogenic contributors involve HLA-B27, the IL-23/IL-17 pathway, and dysregulated tissue-specific cells, reflecting the intricate pathways in disease manifestation.

Despite strides in genetics, immunology, and imaging, significant uncertainties regarding SpA pathogenesis and optimal management strategies remain. This Research Topic aims to elucidate the expanding frontiers of SpA research, amalgamating insights from basic science, translational studies, and clinical practice to explore how bridging autoimmunity and autoinflammation can enhance diagnostic precision and therapeutic targeting.

We aspire to address the multifaceted and intricate character of Spondyloarthritis (SpA), straddling between autoimmunity and autoinflammation. Known pathways including HLA-B27 misfolding and the IL-23/IL-17 axis have been spotlighted, yet the nuanced interactions between innate and adaptive immune cells such as T cells, macrophages, innate lymphoid cells, and γδ T cells are only partially deciphered. Additionally, IL-17's regulatory functions expand beyond immune modulation, impacting structural cells like fibroblasts, osteoblasts, epithelium, and chondrocytes, culminating in synovial inflammation and pathological bone formation, hallmarks of SpA.

Recent progress in therapeutics, including IL-12/23 and IL-17 inhibitors and synthetic options like JAK inhibitors, pave new paths beyond traditional TNF blockades, fostering hope for more tailored treatments.

This Research Topic calls for original research and reviews spanning basic immunology, translational science, and clinical practice, aiming to delve deeper into SpA pathogenesis and value current therapeutic strategies.

To gather further insights into the immunopathogenic mechanisms, clinical features, and therapeutic strategies in Spondyloarthritis (SpA), with an emphasis on bridging autoimmunity and autoinflammation, we welcome articles addressing, but not limited to, the following themes:

- Immune mechanisms and pathogenesis: IL-17/IL-23 axis, Th17 cells, innate immunity, and microbiota.
- Diagnosis and classification: biomarkers, imaging, and immune profiling in various SpA phenotypes.
- Genetics and epigenetics: HLA-B27, genetic susceptibility, and epigenetic regulation.
- Therapeutic strategies: IL-17, IL-23 inhibitors, JAK inhibitors, and personalized medicine.
- Animal models and preclinical insights: models reflecting SpA features and translational research.
- Comorbidities and systemic manifestations: uveitis, psoriasis, IBD, neuroimmune modulation, and chronic stress.
- Immune regulation by stromal and parenchymal cells: fibroblasts, epithelium, osteoblasts, and chondrocytes.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Conceptual Analysis
• Editorial
• FAIR² Data
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Conceptual Analysis
• Editorial
• FAIR² Data
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Systematic Review
• Technology and Code

Keywords: Spondyloarthritis, Autoimmunity, Autoinflammation, HLA-B27, Th17/IL-23 Axis, Inflammasome, Microbiota, Innate immunity, Biologic therapy, Systemic inflammation

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.