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Susceptibility to ankylosing spondylitis (AS) is polygenic with more than 100 genes identified to date. These include HLA-B27 and the aminopeptidases (ERAP1, ERAP2, and LNPEPS), which are involved in antigen processing and presentation to T-cells, and several genes (IL23R, IL6R, STAT3, JAK2, IL1R1/2, IL12B, and IL7R) involved in IL23 driven pathways of inflammation. AS is also strongly associated with polymorphisms in two transcription factors, RUNX3 and T-bet (encoded by TBX21), which are important in T-cell development and function. The influence of these genes on the pathogenesis of AS and their potential for identifying drug targets is discussed here.

Original publication

DOI

10.3389/fimmu.2018.03132

Type

Journal article

Journal

Frontiers in immunology

Publication Date

01/2018

Volume

9

Addresses

Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, United Kingdom.

Keywords

Killer Cells, Natural, CD8-Positive T-Lymphocytes, Humans, Spondylitis, Ankylosing, Aminopeptidases, T-Box Domain Proteins, Receptors, Interleukin, Immunologic Factors, HLA-B27 Antigen, Gene Expression Regulation, Polymorphism, Single Nucleotide, Core Binding Factor Alpha 3 Subunit, Interleukin-23, Molecular Targeted Therapy