Alloreactive donor T cells against host minor histocompatibility antigens (mHAs) cause graft-versus-host disease (GVHD) after marrow transplantation from HLA-identical siblings. We sought to identify and expand regulatory CD4 T cells (Tregs) specific for human mHAs in numbers and potency adequate for clinical testing. Purified Tregs from normal donors were stimulated by dendritic cells (DCs) from their HLA-matched siblings in the presence of interleukin 2, interleukin 15, and rapamycin. Male-specific Treg clones against H-Y antigens DBY, UTY, or DFFRY-2 suppressed conventional CD4 T cell (Tconv) response to the specific antigen. In the blood of 16 donors, we found a 24-fold (range, 8-fold to 39-fold) excess Tconvs over Tregs reactive against sibling mHAs. We expanded mHA-specific Tregs from 4 blood samples and 4 leukaphereses by 155- to 405-fold. Cultured Tregs produced allospecific suppression, maintained demethylation of the Treg-specific Foxp3 gene promoter, Foxp3 expression, and transforming growth factor β production. The rare CD4 T conv and CD8 T cells in the end product were anergic. This is the first report of detection and expansion of potent mHA-specific Tregs from HLA-matched siblings in sufficient numbers for application in human transplant trials.

译文

从HLA相同的兄弟姐妹进行骨髓移植后,针对宿主次要组织相容性抗原 (mha) 的同种反应性供体T细胞会引起移植物抗宿主病 (GVHD)。我们试图鉴定和扩大人类mhs特异性调节性CD4 T细胞 (Tregs) 的数量和效力,足以进行临床测试。在白介素2,白介素15和雷帕霉素的存在下,来自正常供体的纯化treg被其HLA匹配的兄弟姐妹的树突状细胞 (dc) 刺激。针对h-y抗原DBY、UTY或DFFRY-2的男性特异性Treg克隆抑制了对特异性抗原的常规cd4t细胞 (Tconv) 反应。在16位献血者的血液中,我们发现对同胞mh反应的treg的tconv过量为24倍 (范围为8倍至39倍)。我们将来自4个血液样本和4个白细胞的mHA特异性treg扩大了155至405倍。培养的Tregs产生同种特异性抑制,维持Treg特异性Foxp3基因启动子的去甲基化,Foxp3表达和转化生长因子 β 的产生。终产物中罕见的CD4 T conv和CD8 T细胞是无能的。这是从HLA匹配的兄弟姐妹中检测和扩展有效的mHA特异性treg的第一份报告,其数量足以应用于人类移植试验。

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