TY  - JOUR
ID  - open970
UR  - http://www.sciencedirect.com/science/article/pii/S0014579304010385
IS  - 1-3
A1  - Luthra-Guptasarma, Manni
A1  - Singh, Balvinder
N2  - Expression of the MHC class I allele, HLA-B27, is correlated with autoimmune disease. The misfolding and association of B27 heavy chains through non-native disulfide bonds has recently been implicated. Here, we propose that beta2m-free, peptide-free heavy chains support a helix-coil transition in the segment leading from the alpha2 domain to the alpha3 domain, facilitating rotation of backbone angles around residues 167/168, and allowing residues 169-181 (identical to a known B27 ligand) to loop around and occupy the molecule's own peptide-binding cleft. Such 'auto-display', occurring either within B27 molecules, or between B27 molecules, could provoke autoimmune attack.
VL  - 575
TI  - HLA-B27 lacking associated beta2-microglobulin rearranges to auto-display or cross-display residues 169-181: a novel molecular mechanism for spondyloarthropathies.
AV  - restricted
EP  - 8
N1  - Copyright of this article belongs to Elsevier Science.
Y1  - 2004/09/24/
PB  - Elsevier Science
JF  - FEBS letters
KW  - HLA-B27; Ankylosing spondylitis; Protein misfolding; Detailed molecular mechanism; MHC auto display; Autoimmune disorders
SN  - 0014-5793
SP  - 1
ER  -