Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Most nuclear systemic autoantigens are extremely disordered proteins: implications for the etiology of systemic autoimmunity. | Available online http content 7 6 R1360 Research article Most nuclear systemic autoantigens are extremely disordered proteins implications for the etiology of systemic autoimmunity Philip L Carl1 Brenda RS Temple2 and Philip L Cohen3 Department of Pharmacology University of North Carolina Chapel Hill NC 27599 USA 2R. L. Juliano Structural Bioinformatics Core Facility University of North Carolina Chapel Hill NC 27599 USA 3Division of Rheumatology University of Pennsylvania School of Medicine and Philadelphia VA Medical Center Philadelphia PA 19104 USA Corresponding author Philip L Carl plc@ Received 25 Apr 2005 Revisions requested 2 Jun 2005 Revisions received 4 Aug 2005 Accepted 31 Aug 2005 Published 6 Oct 2005 Arthritis Research Therapy 2005 7 R1360-R1374 DOI ar1832 This article is online at http content 7 6 R1360 2005 Carl et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Patients with systemic autoimmune diseases usually produce high levels of antibodies to self-antigens autoantigens . The repertoire of common autoantigens is remarkably limited yet no readily understandable shared thread links these apparently diverse proteins. Using computer prediction algorithms we have found that most nuclear systemic autoantigens are predicted to contain long regions of extreme structural disorder. Such disordered regions would generally make poor B cell epitopes and are predicted to be under-represented as potential T cell epitopes. Consideration of the potential role of protein disorder may give novel insights into the possible role of molecular mimicry in the pathogenesis of autoimmunity. The recognition of extreme autoantigen protein .
