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: Complement and arthritis: another step in understanding. | Available online http content 10 1 104 Editorial Complement and arthritis another step in understanding Michael M Frank and C Garren Hester Department of Pediatrics Duke University Medical Center Durham NC 27710 USA Corresponding author Michael M Frank frank007@ Published 19 February 2008 Arthritis Research Therapy 2008 10 104 doi ar2359 This article is online at http content 10 1 104 2008 BioMed Central Ltd See related research article by Wenderfer et al. http content 9 5 R114 Abstract In a recent research article in Arthritis Research and Therapy Analysis of C204 and the C4 binding protein in the MRL lpr mouse Wenderfer and colleagues report that deficiency in C4 binding protein a down-regulator of the classic pathway of complement does not affect the development of autoimmune disease. These data support the earlier finding that the alternative pathway and not the classic pathway drives disease progression. However in a milder variant of the MRL lpr model the lpr lpr mouse classic pathway deficiency does contribute toward renal pathology and more severe disease. In this editorial we discuss the factors that may cause such a discrepancy. In a previous issue of Arthritis Research and Therapy Wenderfer and colleagues 1 analysed the C4 and the C4 binding protein in the MLR lpr mouse a well-studied model of immune complex disease with autoimmune tissue damage 2 . The lpr mutation confers a defect in Fas with resulting failure of cellular apoptosis and the MRL defects predispose the mouse to the development of autoimmunity. At an early age these mice develop massive lymphadenopathy lupus like antibodies and severe tissue damage. Organ pathology results in part from the formation and organ deposition of immune complexes the activation of complement and consequent tissue damage. Previous work has shown that much of this damage is a result of alternative complement pathway AP .
