tailieunhanh - Báo cáo y học: "Interleukin-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates interleukin-17A and RORγt in γδ T cells"

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: Interleukin-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates interleukin-17A and RORγt in γδ T cells. | Available online http content 11 6 R194 Research article Interleukin-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates interleukin-17A and RORyt in ỴÔ T cells Ferry Cornelissen1 2 Adriana MC Mus1 2 Patrick S Asmawidjaja1 2 Jan Piet van Hamburg1 2 Joel Tocker3 and Erik Lubberts1 2 Open Access Department of Rheumatology Erasmus Medical Center Rotterdam Dr. Molewaterplein 50 Rotterdam 3015 GE the Netherlands department of Immunology Erasmus Medical Center Rotterdam Dr. Molewaterplein 50 Rotterdam 3015 GE the Netherlands 3Amgen Inc. 51 University Street Seattle WA 98101-2918 USA Corresponding author Erik Lubberts Received 19 Aug 2009 Revisions requested 6 Oct 2009 Revisions received 16 Nov 2009 Accepted 1 7 Dec 2009 Published 17 Dec 2009 Arthritis Research Therapy 2009 11 R194 doi 86 ar2893 This article is online at http content 11 6 R194 2009 Cornelissen 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. Abstract Introduction Interleukin IL -23 is essential for the development of various experimental autoimmune models. However the role of IL-23 in non-autoimmune experimental arthritis remains unclear. Here we examined the role of IL-23 in the non-autoimmune antigen-induced arthritis AIA model. In addition the regulatory potential of IL-23 in IL-17A and retinoic acid-related orphan receptor gamma t RORyt expression in CD4 and TCRyS T cells was evaluated systemically as well as at the site of inflammation. Methods Antigen-induced arthritis was induced in wild-type IL-23p19-deficient and IL-17 Receptor A - knockout mice. At different time points synovial cytokine and chemokine expression was measured. At