Ankylosing spondylitis (AS) is an immune-mediated rheumatic disorder primarily affecting the axial skeleton and sacroiliac joints. This disease is the prototype of a group of conditions called Spondyloarthritis, encompassing reactive arthritis, psoriatic arthritis and arthritis associated with inflammatory bowel disease. Chronic inflammation along with bone resorption and new bone formation are the pathogenic hallmarks of this disease. However, the underlying mechanisms remain poorly defined and are currently under the focus of intense investigation.
There is a strong link between genetic background and susceptibility to AS, with more than 100 allelic risk variants identified so far. The strong association of AS with HLA-B27 and, as more recently discovered, with ERAP1 and ERAP2 genes, points to antigen presentation as a causative event. Data from humans and animal models indicate that different cell types belonging to both innate and adaptive immune systems may be involved in AS pathogenesis. Several genetic and functional studies and clinical trials have converged on the IL-23R/IL-17 axis, directing attention to the Th17 subset and other IL-17 producing cells such as innate lymphoid cells (ILCs). Accordingly, clinical use of IL-17 and TNF inhibitors have shown therapeutic benefits in AS patients and have remarkably improved the treatment of this disease. Finally, the presence of sub-clinical intestinal inflammation in the majority of AS patients also suggests that the microbiota may be an additional player in the pathogenesis of this disease. We are therefore facing a complex and still enigmatic disease for which the understanding of the molecular mechanisms involved can benefit from system biology approaches.
In this Research topic, we aim to collect a series of articles that will provide a comprehensive overview of basic as well as translational research on-going in the field of AS. In particular, studies ranging from immunogenetics and functional genomics to the analysis of immune-mediated pathophysiologic mechanisms involving bone, joint, gut, skin and eye, are encouraged. We welcome the submission of Reviews, Mini-Reviews, Hypothesis and Perspective articles covering, but not limited to, the following topics:
1. Innate and adaptive immunity involved in AS and related Spondyloarthritis.
2. Genetics and functional genomics of AS and related Spondyloarthritis.
3. Pathobiology of HLA-B27 in the onset of AS.
4. Lessons from other HLA-class I mediated autoimmune/autoinflammatory diseases.
5. Immuno-metabolism of the microenvironment in AS-inflamed tissues.
6. The intestine/bone axis in AS: the role of different cell types, cellular trafficking and crosstalk.
7. Animal models for studying Spondyloarthritis and for exploring new therapeutic approaches.
8. Biomarkers for diagnosis of AS, disease activity and prediction of response to therapy.
9. The role of the microbiota in AS and related Spondyloarthritis.
10. Translational perspectives in Spondyloarthritis.
Ankylosing spondylitis (AS) is an immune-mediated rheumatic disorder primarily affecting the axial skeleton and sacroiliac joints. This disease is the prototype of a group of conditions called Spondyloarthritis, encompassing reactive arthritis, psoriatic arthritis and arthritis associated with inflammatory bowel disease. Chronic inflammation along with bone resorption and new bone formation are the pathogenic hallmarks of this disease. However, the underlying mechanisms remain poorly defined and are currently under the focus of intense investigation.
There is a strong link between genetic background and susceptibility to AS, with more than 100 allelic risk variants identified so far. The strong association of AS with HLA-B27 and, as more recently discovered, with ERAP1 and ERAP2 genes, points to antigen presentation as a causative event. Data from humans and animal models indicate that different cell types belonging to both innate and adaptive immune systems may be involved in AS pathogenesis. Several genetic and functional studies and clinical trials have converged on the IL-23R/IL-17 axis, directing attention to the Th17 subset and other IL-17 producing cells such as innate lymphoid cells (ILCs). Accordingly, clinical use of IL-17 and TNF inhibitors have shown therapeutic benefits in AS patients and have remarkably improved the treatment of this disease. Finally, the presence of sub-clinical intestinal inflammation in the majority of AS patients also suggests that the microbiota may be an additional player in the pathogenesis of this disease. We are therefore facing a complex and still enigmatic disease for which the understanding of the molecular mechanisms involved can benefit from system biology approaches.
In this Research topic, we aim to collect a series of articles that will provide a comprehensive overview of basic as well as translational research on-going in the field of AS. In particular, studies ranging from immunogenetics and functional genomics to the analysis of immune-mediated pathophysiologic mechanisms involving bone, joint, gut, skin and eye, are encouraged. We welcome the submission of Reviews, Mini-Reviews, Hypothesis and Perspective articles covering, but not limited to, the following topics:
1. Innate and adaptive immunity involved in AS and related Spondyloarthritis.
2. Genetics and functional genomics of AS and related Spondyloarthritis.
3. Pathobiology of HLA-B27 in the onset of AS.
4. Lessons from other HLA-class I mediated autoimmune/autoinflammatory diseases.
5. Immuno-metabolism of the microenvironment in AS-inflamed tissues.
6. The intestine/bone axis in AS: the role of different cell types, cellular trafficking and crosstalk.
7. Animal models for studying Spondyloarthritis and for exploring new therapeutic approaches.
8. Biomarkers for diagnosis of AS, disease activity and prediction of response to therapy.
9. The role of the microbiota in AS and related Spondyloarthritis.
10. Translational perspectives in Spondyloarthritis.
