作者: Q. Shi , J. R. Lees , D. W. Scott , D. L. Farber , S. T. Bartlett
DOI: 10.1111/J.1600-6143.2011.03943.X
关键词:
摘要: Donor pancreatic lymph node cells (PLNC) protect islet transplants in Non-obese diabetic (NOD) mice. We hypothesized that induced FoxP3+ regulatory T (Tregs) were required for long-term engraftment. NOD or NOD.NON mice treated with ALS (antilymphocyte serum) and transplanted NOR islets +/–PLNC (5 × 107). In vivo proliferation expansion of Tregs was monitored spleen PLN from ALS- ALS/PLNC-treated recipient Anti-CD25 depletion used to determine the necessity tolerance. numbers significantly increased recipients compared ALS-treated mice, recipient-derived localized islets, this associated intact, insulin-producing β cells. Proliferation markedly PLNC-treated accepted grafts, but not receiving PLNC. Deletion anti-CD25 antibodies prevented graft tolerance resulted rejection. Adoptive transfer secondary NOD.scid inhibited autoimmunity by cotransferred effector Treg ALS/PLNC-treatment promoted long term survival. Strategies leading localization transplant site represent a therapeutic approach controlling recurrent autoimmunity.