Genetic risk factors in ankylosing spondylitis: Insights into etiology and disease pathogenesis
Author:
Affiliation:
1. Centre for Nanosciences and Molecular Medicine Amrita Vishwa Vidyapeetham Kochi India
2. Department of Rheumatology, Amrita Institute of Medical Sciences and Research Centre Amrita Vishwa Vidyapeetham Kochi India
Publisher
Wiley
Subject
Rheumatology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1111/1756-185X.15023
Reference33 articles.
1. Revisiting the Arthritogenic Peptide Theory: Quantitative Not Qualitative Changes in the Peptide Repertoire of HLA-B27 Allotypes
2. Association of gut inflammation with increased serum IgA class Klebsiella antibody concentrations in patients with axial ankylosing spondylitis (AS): implication for different aetiopathogenetic mechanisms for axial and peripheral AS?
3. Interaction of HLA-B27 homodimers with KIR3DL1 and KIR3DL2, unlike HLA-B27 heterotrimers, is independent of the sequence of bound peptide
4. KIR3DL2 Binds to HLA-B27 Dimers and Free H Chains More Strongly than Other HLA Class I and Promotes the Expansion of T Cells in Ankylosing Spondylitis
5. The ER aminopeptidase, ERAP1, trims precursors to lengths of MHC class I peptides by a "molecular ruler" mechanism
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