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[通过混合淋巴细胞反应和细胞介导的淋巴细胞溶解分析肾移植受者的特异性细胞免疫]

[Analysis of specific cellular immunity in renal transplant recipients by MLR & CML].

作者信息

Seki Y

出版信息

Nihon Geka Gakkai Zasshi. 1983 Jun;84(6):488-99.

PMID:6232457
Abstract

The specific cellular immunity of renal transplant recipients was investigated by MLR & CML. MLR has been thought to reflect the disparity of HLA-D locus between two individuals and CML to represent an in vitro model for graft rejection and graft adaptation. Anti-donor and anti-control reactivities were diminished in MLR immediately after transplantation even during acute rejection. These MLR suppression are probably due to immuno-suppressive drugs. In acute rejection episode, CML reactivity against donor was elevated and well correlated with clinical findings, but on the other hand, MLR reactivity was suppressed. This discrepancy indicates that strong MLR is not needed to induce high CML. The in vitro development of cytotoxic T cells as a result of proliferation in MLR is impaired in long term survivors and quiescent recipients after transplantation. These suppression is directed to specific donor but not to unrelated third party cells. I have demonstrated the MHC restricted CML suppressor T cell by using HLA identical monozygous twin's lymphocyte. This suppressor T cell may prove to be of value in enhancing graft acceptance and play a part of immunomodulations.

摘要

采用混合淋巴细胞反应(MLR)和细胞介导的淋巴细胞毒试验(CML)对肾移植受者的特异性细胞免疫进行了研究。人们一直认为MLR反映了两个个体之间HLA - D位点的差异,而CML代表了移植排斥和移植适应的体外模型。即使在急性排斥反应期间,移植后即刻的MLR中抗供体和抗对照反应性也会降低。这些MLR抑制可能是由于免疫抑制药物所致。在急性排斥反应发作时,针对供体的CML反应性升高,且与临床发现密切相关,但另一方面,MLR反应性受到抑制。这种差异表明,诱导高CML并不需要强烈的MLR。在长期存活者和移植后静止的受者中,由于MLR中细胞增殖导致的细胞毒性T细胞的体外发育受到损害。这些抑制作用针对特定的供体细胞,而不是无关的第三方细胞。我通过使用HLA相同的同卵双胞胎淋巴细胞证明了MHC限制的CML抑制性T细胞。这种抑制性T细胞可能在增强移植接受方面具有价值,并发挥免疫调节作用。

相似文献

1
[Analysis of specific cellular immunity in renal transplant recipients by MLR & CML].[通过混合淋巴细胞反应和细胞介导的淋巴细胞溶解分析肾移植受者的特异性细胞免疫]
Nihon Geka Gakkai Zasshi. 1983 Jun;84(6):488-99.
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[Immunological analysis of mixed lymphocyte culture reaction inhibitory factor induced by donor specific blood transfusions in potential kidney transplant patients].[潜在肾移植患者中供体特异性输血诱导的混合淋巴细胞培养反应抑制因子的免疫学分析]
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Donor-specific T-cell reactivity identifies kidney transplant patients in whom immunosuppressive therapy can be safely reduced.供体特异性T细胞反应性可识别出能够安全减少免疫抑制治疗的肾移植患者。
Transplantation. 2000 Jul 15;70(1):136-43.
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Inhibition of IL-2 synthesis by donor-specific suppressor T cells in a renal transplant recipient.肾移植受者中供体特异性抑制性T细胞对白细胞介素-2合成的抑制作用。
Transpl Int. 1994;7 Suppl 1:S629-33. doi: 10.1111/j.1432-2277.1994.tb01460.x.
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Comparison of cell-mediated lympholysis and mixed lymphocyte culture in the immunologic evaluation for renal transplantation.细胞介导的淋巴细胞溶解与混合淋巴细胞培养在肾移植免疫评估中的比较。
J Immunol. 1982 Oct;129(4):1573-7.
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Renal transplant patients treated with total lymphoid irradiation show specific unresponsiveness to donor antigens the mixed leukocyte reaction (MLR).接受全淋巴照射治疗的肾移植患者对供体抗原混合淋巴细胞反应(MLR)表现出特异性无反应性。
J Immunol. 1987 Jun 1;138(11):3746-50.
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Effect of selective T cell depletion of host and/or donor bone marrow on lymphopoietic repopulation, tolerance, and graft-vs-host disease in mixed allogeneic chimeras (B10 + B10.D2----B10).宿主和/或供体骨髓选择性T细胞清除对混合异基因嵌合体(B10 + B10.D2----B10)中淋巴细胞再填充、耐受性及移植物抗宿主病的影响
J Immunol. 1986 Jan;136(1):28-33.
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Low circulating regulatory T-cell levels after acute rejection in liver transplantation.肝移植急性排斥反应后循环调节性T细胞水平降低。
Liver Transpl. 2006 Feb;12(2):277-84. doi: 10.1002/lt.20612.
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Analysis of the donor-specific cytotoxic T lymphocyte repertoire in a patient with a long term surviving allograft. Frequency, specificity, and phenotype of donor-reactive T cell receptor (TCR)-alpha beta+ and TCR-gamma delta+ clones.长期存活同种异体移植患者供体特异性细胞毒性T淋巴细胞库分析。供体反应性T细胞受体(TCR)αβ⁺和TCRγδ⁺克隆的频率、特异性和表型。
J Immunol. 1990 Feb 15;144(4):1288-94.
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Adoptive transfusion of ex vivo donor alloantigen-stimulated CD4(+)CD25(+) regulatory T cells ameliorates rejection of DA-to-Lewis rat liver transplantation.体外供体同种异体抗原刺激的CD4(+)CD25(+)调节性T细胞的过继性输血可改善DA到Lewis大鼠肝移植的排斥反应。
Surgery. 2007 Jul;142(1):67-73. doi: 10.1016/j.surg.2007.02.014.

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