Krupnick Alexander Sasha, Gelman Andrew E, Barchet Winfried, Richardson Steve, Kreisel Friederike H, Turka Laurence A, Colonna Marco, Patterson G Alexander, Kreisel Daniel
Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Immunol. 2005 Nov 15;175(10):6265-70. doi: 10.4049/jimmunol.175.10.6265.
Unlike graft-resident donor-derived hemopoietic APCs, which decrease in number over time after transplantation, vascular endothelial cells are lifelong residents of a vascularized allograft. Endothelial cells are potent APCs for allogeneic CD8+ T lymphocytes but are unable to induce proliferation of allogeneic CD4+ T lymphocytes. Although the reason for this differential response has been poorly understood, here we report that alloantigen presentation by vascular endothelium to CD4+ T lymphocytes activates and induces CD4+25+Foxp3+ regulatory T cells, which can inhibit proliferation of alloreactive T cells both in vitro and in vivo. This process occurs independently of B7.1 costimulation but is dependent on programmed death ligand 1 (B7-H1). This finding may have important implications for tolerance induction in transplantation.
与移植后数量随时间减少的移植物驻留供体来源的造血抗原呈递细胞不同，血管内皮细胞是血管化同种异体移植物的终身驻留者。内皮细胞是同种异体CD8 + T淋巴细胞的有效抗原呈递细胞，但无法诱导同种异体CD4 + T淋巴细胞增殖。尽管对这种差异反应的原因了解甚少，但我们在此报告，血管内皮向CD4 + T淋巴细胞呈递同种异体抗原会激活并诱导CD4 + 25 + Foxp3 +调节性T细胞，后者可在体外和体内抑制同种反应性T细胞的增殖。此过程独立于B7.1共刺激发生，但依赖于程序性死亡配体1（B7-H1）。这一发现可能对移植中的耐受诱导具有重要意义。
