HLA-B27 misfolding and ankylosing spondylitis

Understanding how HLA-B27 contributes to the pathogenesis of spondyloarthritis continues to be an important goal. Current efforts are aimed largely on three areas of investigation; peptide presentation to CD8T cells, abnormal forms of the HLA-B27 heavy chain and their recognition by leukocyte immuno...

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Veröffentlicht in:	Molecular immunology 2014-01, Vol.57 (1), p.44-51
Hauptverfasser:	Colbert, Robert A., Tran, Tri M., Layh-Schmitt, Gerlinde
Format:	Artikel
Sprache:	eng
Schlagworte:	alleles Animals Ankylosing spondylitis Autophagy bioactive properties endoplasmic reticulum Endoplasmic Reticulum Stress gastrointestinal system gene expression regulation gene overexpression Heat-Shock Proteins - metabolism HLA-B27 Antigen - chemistry HLA-B27 Antigen - genetics HLA-B27 Antigen - metabolism Humans immunologic receptors Interferon-beta - metabolism interleukin-1alpha Interleukin-1alpha - metabolism Interleukin-23 - metabolism macrophages MHC class I monocytes osteoclasts pathogenesis patients Polymorphism, Single Nucleotide Protein Folding Protein misfolding Rats signal transduction Spondylitis, Ankylosing - genetics Spondylitis, Ankylosing - metabolism Spondyloarthritis transgenic animals translation (genetics) ubiquitin ubiquitin-protein ligase Ubiquitin-Protein Ligases - metabolism Unfolded Protein Response
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