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重新审视移植前输血:CD4+调节性T细胞的作用?

Pretransplant blood transfusions revisited: a role for CD(4+) regulatory T cells?

作者信息

Roelen Dave, Brand Anneke, Claas Frans H J

机构信息

Department of Immunohematology and Bloodtransfusion, Leiden University Medical Center, Leiden, The Netherlands.

出版信息

Transplantation. 2004 Jan 15;77(1 Suppl):S26-8. doi: 10.1097/01.TP.0000106469.12073.01.

DOI:10.1097/01.TP.0000106469.12073.01
PMID:14726766
Abstract

Pretransplant blood transfusions have been shown to improve organ allograft survival. However, the immunologic mechanism leading to this beneficial effect of blood transfusions is still unknown. The observation that transfusions sharing at least one HLA-DR antigen (human leukocyte antigen) with the recipient are more effective than HLA-mismatched transfusions has led to the hypothesis that CD(4+) regulatory T cells are induced that recognize allopeptides of the blood transfusion donor in the context of the self-HLA-DR molecule on the donor cells. In vitro studies showed that CD(4+) T cells recognizing an allopeptide in the context of self-HLA-DR are indeed able to decrease the alloimmune response of autologous T cells by affecting the activated T cells directly or indirectly by their modulatory effect on dendritic cells. The first studies in a patient with a well-functioning kidney graft after receiving an HLA-DR-matched pretransplant blood transfusion showed that the low organ donor-specific cytotoxic T-lymphocyte response after transplantation was indeed attributable to the activity of regulatory CD(4+) T cells.

摘要

移植前输血已被证明可提高器官移植存活率。然而,导致输血产生这种有益效果的免疫机制仍不清楚。与受者至少共享一种HLA - DR抗原(人类白细胞抗原)的输血比HLA不匹配的输血更有效的观察结果,引发了一种假说,即诱导产生了CD(4+)调节性T细胞,这些细胞在供体细胞上自身HLA - DR分子的背景下识别输血供体的异源肽。体外研究表明,在自身HLA - DR背景下识别异源肽的CD(4+) T细胞确实能够通过直接影响活化的T细胞或通过其对树突状细胞的调节作用间接降低自体T细胞的同种免疫反应。对一名接受HLA - DR匹配的移植前输血后肾移植功能良好的患者进行的首批研究表明,移植后低水平的器官供体特异性细胞毒性T淋巴细胞反应确实归因于调节性CD(4+) T细胞的活性。

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Pretransplant blood transfusions revisited: a role for CD(4+) regulatory T cells?重新审视移植前输血:CD4+调节性T细胞的作用?
Transplantation. 2004 Jan 15;77(1 Suppl):S26-8. doi: 10.1097/01.TP.0000106469.12073.01.
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