As the prototype of spondyloarthritis, ankylosing spondylitis (AS) is a chronic inflammatory disease that affects the spine and sacroiliac joints. In China, the prevalence of AS is 0.25% - 0.45%. AS can be attributed to both hereditary and environmental factors. 20% - 40% of AS patients reported family history of AS, suggesting the pivotal role of genetic factors in the pathogenesis of AS. Researchers have found a strong association between HLA-B27 and a perpetual activation of both the innate and the adaptive immune systems, in particular of the IL-23/IL-17 axis and Th1 effector T-cell lineage with the overproduction of tumor necrosis factor-a (TNF-a). Humans and animal studies have also suggested the important role of T-cell mediated immune regulation in AS susceptibility. However, the precise etiology of AS remains poorly studied and merits further investigations.
Rapid progress in immunology and genetics have not only revealed the role of innate and adaptive immune cells in the triggering, initiation, development, and regulation of AS, but also shed light on mechanisms associated with resistance to AS therapy. This Research Topic aims at bringing together recent advances on the pathogenesis of AS to provide a theoretical basis for the development of new diagnostic methods, therapeutic modalities, and cell therapy technologies. Imaging and omics studies screening novel biomarkers in clinical practice predicting response to AS therapeutics (such as targeted IL-17 inhibitors) are also welcome. We welcome submissions of Original Research, Reviews, Mini-reviews, covering but not limited to, the following topics:
1. Innate and adaptive immune responses in AS
2. The relationship between susceptibility genes (e.g. ANO6) and bone metabolism/immune regulation
3. Genetic variations associated with AS and major immune signaling pathways involved in AS identified by -omics studies
4. HLA-B27 subtypes involved in immune regulation of AS
5. Novel therapeutic strategies of AS targeting immune cells
As the prototype of spondyloarthritis, ankylosing spondylitis (AS) is a chronic inflammatory disease that affects the spine and sacroiliac joints. In China, the prevalence of AS is 0.25% - 0.45%. AS can be attributed to both hereditary and environmental factors. 20% - 40% of AS patients reported family history of AS, suggesting the pivotal role of genetic factors in the pathogenesis of AS. Researchers have found a strong association between HLA-B27 and a perpetual activation of both the innate and the adaptive immune systems, in particular of the IL-23/IL-17 axis and Th1 effector T-cell lineage with the overproduction of tumor necrosis factor-a (TNF-a). Humans and animal studies have also suggested the important role of T-cell mediated immune regulation in AS susceptibility. However, the precise etiology of AS remains poorly studied and merits further investigations.
Rapid progress in immunology and genetics have not only revealed the role of innate and adaptive immune cells in the triggering, initiation, development, and regulation of AS, but also shed light on mechanisms associated with resistance to AS therapy. This Research Topic aims at bringing together recent advances on the pathogenesis of AS to provide a theoretical basis for the development of new diagnostic methods, therapeutic modalities, and cell therapy technologies. Imaging and omics studies screening novel biomarkers in clinical practice predicting response to AS therapeutics (such as targeted IL-17 inhibitors) are also welcome. We welcome submissions of Original Research, Reviews, Mini-reviews, covering but not limited to, the following topics:
1. Innate and adaptive immune responses in AS
2. The relationship between susceptibility genes (e.g. ANO6) and bone metabolism/immune regulation
3. Genetic variations associated with AS and major immune signaling pathways involved in AS identified by -omics studies
4. HLA-B27 subtypes involved in immune regulation of AS
5. Novel therapeutic strategies of AS targeting immune cells
