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Updated: May 8, 2026
04:47
Du-Moxibustion in a Mouse Model of Ankylosing Spondylitis
Published on: October 27, 2023
Ankylosing spondylitis: from cells to genes.
José Francisco Zambrano-Zaragoza1, Juan Manuel Agraz-Cibrian, Christian González-Reyes
1Universidad Autónoma de Nayarit, Unidad Académica de Ciencias Químico Biológicas y Farmacéuticas, CP. 63190 Tepic Nay., Mexico.
International Journal of Inflammation
|August 24, 2013
Summary
Ankylosing spondylitis (AS) is an autoimmune disease. This review examines the role of HLA-B27, immune cells like Th17, and genetic factors in AS pathogenesis.
Area of Science:
- Immunology
- Genetics
- Rheumatology
Background:
- Ankylosing spondylitis (AS) is a chronic autoimmune inflammatory disease with unknown causes.
- HLA-B27 is a significant genetic risk factor, but its precise role in AS pathogenesis remains unclear.
- Interleukin-17 (IL-17) and Th17 cells are crucial in autoimmunity and inflammation, suggesting their involvement in AS.
Purpose of the Study:
- To review the characteristics of HLA-B27 and proposed mechanisms linking it to AS.
- To analyze the immune response, focusing on Th17 cells, NK cells, and regulatory T cells in AS.
- To identify genes associated with AS and explore potential genetic linkages.
Main Methods:
- Literature review of existing studies on AS pathogenesis.
- Analysis of the role of HLA-B27, IL-17, Th17 cells, and other immune cells.
- Examination of genetic factors, including polymorphisms and mutations, linked to AS.
Main Results:
- HLA-B27 subtypes and their association with AS are extensively studied.
- IL-17 and IL-23 pathways, along with Th17 cell characterization, are implicated in AS.
- Genetic variations in immune response genes have been evaluated for their linkage to AS.
Conclusions:
- Understanding the interplay between HLA-B27, immune cells, and genetic factors is key to unraveling AS pathogenesis.
- Further research into these components may reveal novel therapeutic targets for ankylosing spondylitis.
- This review synthesizes current knowledge on the immunological and genetic underpinnings of AS.
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