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001-es BibID:	BIBFORM049271
Első szerző:	Angyal Adrienn
Cím:	Development of proteoglycan-induced arthritis depends on T cell-supported autoantibody production, but does not involve significant influx of T cells into the joints / Adrienn Angyal, Colt Egelston, Tamás Kobezda, Katalin Olasz, Anna László, Tibor T. Glant, Katalin Mikecz
Dátum:	2010
ISSN:	1478-6354 1478-6362
Megjegyzések:	Introduction: Inflammatory joint destruction in rheumatoid arthritis (RA) may be triggered by autoantibodies, theproduction of which is supported by autoreactive T cells. Studies on RA and animal models of the disease suggestthat T cells recruited in the joints can locally initiate or propagate arthritis. Herein, we investigated the role of jointhomingversus lymphoid organ-homing T cells in the development of proteoglycan-induced arthritis (PGIA), anautoimmune model of RA.Methods: To identify T cells migrating to the joints before and during development of autoimmune arthritis, wetransferred fluorescence-labeled T cells, along with antigen-presenting cells, from BALB/c mice with PGIA to naïvesyngeneic severe combined immunodeficient (SCID) mice. We then monitored the recruitment of donor T cells inthe ankle joints and joint-draining lymph nodes of the recipients using in vivo two-photon microscopy and ex vivodetection methods. To limit T-cell access to the joints, we selectively depleted T cells in the blood circulation bytreatment with FTY720, an inhibitor of lymphocyte egress from lymphoid organs. Reduction of T cell presence inboth lymphoid organs and blood was achieved by injection of donor cells from which T cells were removed priorto transfer. T and B cells were quantitated by flow cytometry, and antigen (PG)-specific responses were assessed bycell proliferation and serum antibody assays.Results: Despite development of adoptively transferred arthritis in the recipient SCID mice, we found very fewdonor T cells in their joints after cell transfer. Treatment of recipient mice with FTY720 left the T-cell pool in thelymphoid organs intact, but reduced T cells in both peripheral blood and joints. However, FTY720 treatment failedto inhibit PGIA development. In contrast, arthritis was not seen in recipient mice after transfer of T cell-depletedcells from arthritic donors, and serum autoantibodies to PG were not detected in this group of mice.Conclusions: Our results suggest that antigen-specific T cells, which home to lymphoid organs and provide helpto B cells for systemic autoantibody production, play a greater role in the development and progression ofautoimmune arthritis than the small population of T cells that migrate to the joints.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Arthritis Research & Therapy. - 12 : 2 (2010), p. R44. -
További szerzők:	Egelston, Colt Kobezda Tamás (1983-) (Ph.D hallgató) Olasz Katalin László Anna Glant Tibor T. Mikecz Katalin
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