Reshaping Cinderellas slipper the shared epitope hypothesis 英文参考文献.docVIP

Available online /content/8/3/109 Commentary Reshaping Cinderella’s slipper: the shared epitope hypothesis Robert Winchester Departments of Medicine, Pediatrics and Pathology, Columbia University, New York, NY 10032, USA Corresponding author: Robert Winchester, rjw8@ Published: 22 May 2006 Arthritis Research Therapy 2006, 8:109 (doi:10.1186/ar1970) This article is online at /content/8/3/109 ? 2006 BioMed Central Ltd See related research article by Michou et al., /content/8/3/R79 Abstract the SE hypothesis came from other unrelated alleles in different populations that encode a SE motif that were This issue of Arthritis Research and Therapy contains a succinct and elegant paper by Michou and colleagues that advances our understanding of the genetic basis of rheumatoid arthritis (RA) by reclassifying the contribution of RA susceptibility alleles according to their structure. This line of research is potentially important in our conceptualization of the mechanism of disease in RA, in predicting disease course and severity, and as a model for further studies on this topic. The author’s approach to reassessing the molecular structure of the shared epitope redirects attention to using the properties of the major histocompatibility complex molecules associated with susceptibility to search for the peptides driving the autoimmune process underlying rheumatoid arthritis identified as RA susceptibility alleles, for example, DRB1*1402 [5] and DRB1*1001 [6]. Although a Google search reveals over 40,000 hits for ‘shared epitope’, reflecting the efforts by many to advance RA genetics, both knowledge of the inciting peptide, and how the nature and conformation of the peptide-binding groove predispose to RA eludes our grasp. Difficulties in identifying which alleles are implicated in RA susceptibility or protection and which regions of molecules encoded by these allele