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: Development of proteoglycan-induced arthritis depends on T cell-supported autoantibody production, but does not involve significant influx of T cells into the joints. | Angyal et al. Arthritis Research Therapy 2010 12 R44 http content 12 2 R44 RESEARCH ARTICLE Open Access Development of proteoglycan-induced arthritis depends on T cell-supported autoantibody production but does not involve significant influx of T cells into the joints 1 f 2f 1 1 1 1 1 Adrienn Angyal Colt Egelston Tamás Kobezda Katalin Olasz Anna László Tibor T Glant Katalin Mikecz Abstract Introduction Inflammatory joint destruction in rheumatoid arthritis RA may be triggered by autoantibodies the production of which is supported by autoreactive T cells. Studies on RA and animal models of the disease suggest that T cells recruited in the joints can locally initiate or propagate arthritis. Herein we investigated the role of jointhoming versus lymphoid organ-homing T cells in the development of proteoglycan-induced arthritis PGIA an autoimmune model of RA. Methods To identify T cells migrating to the joints before and during development of autoimmune arthritis we transferred fluorescence-labeled T cells along with antigen-presenting cells from BALB c mice with PGIA to naive syngeneic severe combined immunodeficient SCID mice. We then monitored the recruitment of donor T cells in the ankle joints and joint-draining lymph nodes of the recipients using in vivo two-photon microscopy and ex vivo detection methods. To limit T-cell access to the joints we selectively depleted T cells in the blood circulation by treatment with FTY720 an inhibitor of lymphocyte egress from lymphoid organs. Reduction of T cell presence in both lymphoid organs and blood was achieved by injection of donor cells from which T cells were removed prior to transfer. T and B cells were quantitated by flow cytometry and antigen PG -specific responses were assessed by cell proliferation and serum antibody assays. Results Despite development of adoptively transferred arthritis in the recipient SCID mice we found very few donor T cells in their joints after cell transfer. Treatment
