tailieunhanh - Báo cáo y học: "Cystatin C influences the autoimmune but not inflammatory response to cartilage type II collagen leading to chronic arthritis development"

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: Cystatin C influences the autoimmune but not inflammatory response to cartilage type II collagen leading to chronic arthritis development. | Băcklund et al. Arthritis Research Therapy 2011 13 R54 http content 13 2 R54 RESEARCH ARTICLE Open Access Cystatin C influences the autoimmune but not inflammatory response to cartilage type II collagen leading to chronic arthritis development A I s I D - lx 11 I X-J 1 2 I_I z I m I s I 1 t D r A I r r z V 3 t ri -I I_I lx s V f r z V 4 5 ỉ r I f I I r I rAA m4 Alexandra BacKlund Meirav HOimaam Ragnar Mattsson Katarina HaKansson veronica Lindstrom Kutty Selva NandaKumar1 Anders Grubb4 and Rikard Holmdahl1 Abstract Introduction Collagen-induced arthritis CIA is a mouse model for rheumatoid arthritis RA and is induced after immunization with type II collagen CII . CIA like RA is an autoimmune disease leading to destruction of cartilage and joints and both the priming and inflammatory phases have been suggested to be dependent on proteases. In particular the cysteine proteases have been proposed to be detrimental to the arthritic process and even immunomodulatory. A natural inhibitor of cysteine proteases is cystatin C. Methods Cystatin C-deficient sufficient and heterozygous mice were tested for onset incidence and severity of CIA. The effect of cystatin C-deficiency was further dissected by testing the inflammatory effector phase of CIA that is collagen antibody-induced arthritis model and priming phase that is T cell response both in vivo and in vitro. In addition in order to determine the importance of T cells and antigen-presenting cells APCs these cell populations were separated and in vitro T cell responses determined in a mixed co-culture system. Finally flow cytometry was used in order to further characterize cell populations in cystatin C-deficient mice. Results Here we show that mice lacking cystatin C develop arthritis at a higher incidence and an earlier onset than wild-type controls. Interestingly when the inflammatory phase of CIA was examined independently from immune priming then cystatin C-deficiency did not enhance the .