Tutschka P J, Hess A D, Beschorner W E, Santos G W
Transplantation. 1981 Sep;32(3):203-9. doi: 10.1097/00007890-198109000-00005.
Histoincompatible-complete radiation chimeras, after resolving acute graft-versus-host disease (GVHD), establish specific tolerance to host and donor alloantigens. This tolerance can be perturbed with immunosuppressive agents and infusions of small numbers of donor-type cells, with infusions of massive numbers of donor-type cells, or with infusions of a small number of donor-type cells, that were sensitized against host antigens prior to transfer. These chimeras possess T lymphocytes in the spleen that specifically suppress donor to host mixed lymphocyte reactions and adoptively transfer suppression of GVHD to secondary hosts. Nylon-wool fractionation of chimeric spleen cells restores the response of chimeric lymphocytes to host alloantigens, suggesting that transplantation tolerance is not attributable to clonal deletion but the activity of nylon-wool-adherent T suppressor spleen cells.
组织不相容性完全辐射嵌合体在解决急性移植物抗宿主病（GVHD）后，会对宿主和供体同种异体抗原建立特异性耐受。这种耐受可被免疫抑制剂、输注少量供体类型细胞、输注大量供体类型细胞或输注少量在转移前已对宿主抗原致敏的供体类型细胞所干扰。这些嵌合体在脾脏中拥有T淋巴细胞，可特异性抑制供体对宿主的混合淋巴细胞反应，并将GVHD抑制作用过继转移至二级宿主。对嵌合脾细胞进行尼龙毛分离可恢复嵌合淋巴细胞对宿主同种异体抗原的反应，这表明移植耐受并非归因于克隆缺失，而是尼龙毛黏附性T抑制性脾细胞的活性。
