Claas F H, de Koster H S, Lagaaij E L, van Rood J J
Department of Immunohaematology and Blood Bank University Hospital, Leiden, The Netherlands.
Exp Nephrol. 1993 Mar-Apr;1(2):134-8.
Pretransplant blood transfusions have been given to renal transplant recipients in order to improve graft survival since almost 20 years. Nevertheless, the mechanism involved in this tolerating effect of blood transfusions has not been revealed yet. Recent data, showing a need for sharing of at least one HLA-DR antigen between blood transfusion donor and recipient to obtain downregulation of the alloimmune response, are the basis of the present hypothesis. We postulate that HLA-DR-shared blood transfusions activate CD4+ T cells recognizing allogeneic peptides in the context of the shared HLA-DR molecule. These CD4+ T cells are able to downregulate the immune response of autologous activated (thus HLA-DR-positive) T cells directed against any allogeneic organ, sharing at least one allogeneic peptide with the blood transfusion donor. Essential in this hypothesis is that the T cells activated by the graft will pick up that allogeneic peptide from the transplanted organ and present it in the context of the shared HLA-DR molecule to the autologous regulatory CD4+ T cells, primed by the blood transfusion.
近20年来，肾移植受者一直接受移植前输血以提高移植物存活率。然而，输血这种耐受作用所涉及的机制尚未阐明。最近的数据表明，输血供者与受者之间至少需要共享一种HLA - DR抗原才能使同种免疫反应下调，这是当前假说的基础。我们推测，共享HLA - DR的输血会激活CD4 + T细胞，这些细胞在共享的HLA - DR分子环境中识别同种异体肽。这些CD4 + T细胞能够下调自体活化（因此HLA - DR呈阳性）T细胞针对任何同种异体器官的免疫反应，该同种异体器官与输血供者至少共享一种同种异体肽。这一假说的关键在于，被移植物激活的T细胞会从移植器官中获取该同种异体肽，并在共享的HLA - DR分子环境中呈递给由输血致敏的自体调节性CD4 + T细胞。
