tailieunhanh - Báo cáo y học: "Direct interaction of immunoglobulins with synovial fibroblasts: a missing link in the pathogenesis of rheumatoid arthritis"

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: Direct interaction of immunoglobulins with synovial fibroblasts: a missing link in the pathogenesis of rheumatoid arthritis? | Arthritis Research Therapy Vol 7 No 1 Pap Viewpoint Direct interaction of immunoglobulins with synovial fibroblasts a missing link in the pathogenesis of rheumatoid arthritis Thomas Pap Division of Molecular Medicine of Musculoskeletal Tissue University Hospital Munster Germany Corresponding author Thomas Pap tpap@ Published 20 December 2004 Arthritis Res Ther 2005 7 44-46 DOI ar1493 2004 BioMed Central Ltd It has been well established that the pathogenesis of rheumatoid arthritis RA comprises three distinct but interdependent phenomena the hyperplasia of synovial tissue chronic inflammation both local and systemic and alterations in the immune response including changes in the T-cell repertoire and the production of autoantibodies 1 . The precise nature of these interactions however particularly the role of autoantibodies in RA pathogenesis is not yet fully understood. Whilst the occurrence of autoantibodies has been recognised as a characteristic feature of disease and certain autoantibodies have become valuable tools for diagnosis their contribution to the initiation and perpetuation of disease has remained largely elusive. A recent article by Terry Smith and William Cruikshank in the Journal of Immunology provides fascinating yet unexpected insights into how autoantibodies contribute to the maintenance of inflammatory disease processes in RA 2 . The authors report that IgG antibodies from the sera of patients with RA RA-IgG can stimulate RA synovial fibroblasts RASFs through interaction with insulin-like growth factor receptor 1 IGF-R1 . This interaction of RA-IgG with IGF-R1 increases the production of IL-16 and RANTES in RASFs provoking chemoattraction of T cells. The data demonstrate for the first time a bridging link between B-cell activity and T-cell trafficking. In addition they are of potential importance for the development of innovative therapeutic strategies in which interrupting the IGF-1 IGF-1R axis could result in sustained .