通过供体脾细胞治疗和延长疗程的抗CD154单克隆抗体诱导的同种异体皮肤移植耐受性增强。 - Suppr

Suppr

超能文献

Improved skin allograft tolerance induced by treatment with donor splenocytes and an extended course of anti-CD154 monoclonal antibody.

作者信息

Markees T, Phillips N, Gordon E, Noelle R J, Mordes J P, Greiner D L, Rossini A A

机构信息

University of Massachusetts Medical School, Worcester, MA 01605, USA.

出版信息

Transplant Proc. 1998 Aug;30(5):2444-6. doi: 10.1016/s0041-1345(98)00680-0.

DOI:10.1016/s0041-1345(98)00680-0

PMID:9723531

Abstract

摘要

相似文献

Improved skin allograft tolerance induced by treatment with donor splenocytes and an extended course of anti-CD154 monoclonal antibody.通过供体脾细胞治疗和延长疗程的抗CD154单克隆抗体诱导的同种异体皮肤移植耐受性增强。

Transplant Proc. 1998 Aug;30(5):2444-6. doi: 10.1016/s0041-1345(98)00680-0.

Prolonged skin allograft survival in mice treated with Flt3-ligand-induced dendritic cells and anti-CD154 monoclonal antibody.用Flt3配体诱导的树突状细胞和抗CD154单克隆抗体处理的小鼠中皮肤同种异体移植物的长期存活

Transplant Proc. 1999 Feb-Mar;31(1-2):884-5. doi: 10.1016/s0041-1345(98)01817-x.

Tolerance to islet xenografts induced by dual manipulation of antigen presentation and co-stimulation.

Transplant Proc. 1996 Apr;28(2):814-5.

Treatment of allograft recipients with donor-specific transfusion and anti-CD154 antibody leads to deletion of alloreactive CD8+ T cells and prolonged graft survival in a CTLA4-dependent manner.用供体特异性输血和抗CD154抗体治疗同种异体移植受者会导致同种异体反应性CD8 + T细胞缺失，并以CTLA4依赖的方式延长移植物存活时间。

J Immunol. 2000 Jan 1;164(1):512-21. doi: 10.4049/jimmunol.164.1.512.

Prolonged survival of rat islet and skin xenografts in mice treated with donor splenocytes and anti-CD154 monoclonal antibody.在用供体脾细胞和抗CD154单克隆抗体处理的小鼠中，大鼠胰岛和皮肤异种移植物的长期存活。

Diabetes. 1998 Aug;47(8):1199-206. doi: 10.2337/diab.47.8.1199.

Long-term survival of skin allografts induced by donor splenocytes and anti-CD154 antibody in thymectomized mice requires CD4(+) T cells, interferon-gamma, and CTLA4.在胸腺切除的小鼠中，供体脾细胞和抗CD154抗体诱导的皮肤同种异体移植物的长期存活需要CD4(+) T细胞、干扰素-γ和CTLA4。

J Clin Invest. 1998 Jun 1;101(11):2446-55. doi: 10.1172/JCI2703.

Increased apoptosis of immunoreactive host cells and augmented donor leukocyte chimerism, not sustained inhibition of B7 molecule expression are associated with prolonged cardiac allograft survival in mice preconditioned with immature donor dendritic cells plus anti-CD40L mAb.在用未成熟供体树突状细胞加抗CD40L单克隆抗体预处理的小鼠中，免疫反应性宿主细胞凋亡增加和供体白细胞嵌合率提高，而非B7分子表达的持续抑制，与心脏同种异体移植的长期存活相关。

Transplantation. 1999 Sep 27;68(6):747-57. doi: 10.1097/00007890-199909270-00006.

Host CD40 ligand deficiency induces long-term allograft survival and donor-specific tolerance in mouse cardiac transplantation but does not prevent graft arteriosclerosis.宿主CD40配体缺陷可诱导小鼠心脏移植中长期移植物存活和供体特异性耐受，但不能预防移植血管硬化。

J Immunol. 2000 Sep 15;165(6):3506-18. doi: 10.4049/jimmunol.165.6.3506.

CTLA4 signals are required to optimally induce allograft tolerance with combined donor-specific transfusion and anti-CD154 monoclonal antibody treatment.CTLA4信号是联合供体特异性输血和抗CD154单克隆抗体治疗以最佳诱导同种异体移植耐受所必需的。

J Immunol. 1999 Apr 15;162(8):4983-90.

Evaluation of donor-specific transfusion sources: unique failure of bone marrow cells to induce prolonged skin allograft survival with anti-CD154 monoclonal antibody.供体特异性输血来源的评估：骨髓细胞在抗CD154单克隆抗体作用下诱导皮肤同种异体移植长期存活的独特失败情况。

Transplantation. 2004 Dec 15;78(11):1601-8. doi: 10.1097/01.tp.0000140847.29917.65.

引用本文的文献

Tryptophan hydroxylase-1 regulates immune tolerance and inflammation.色氨酸羟化酶-1 调节免疫耐受和炎症。

J Exp Med. 2012 Oct 22;209(11):2127-35. doi: 10.1084/jem.20120408. Epub 2012 Sep 24.

Protein kinase C signaling during T cell activation induces the endoplasmic reticulum stress response.T细胞活化过程中的蛋白激酶C信号传导诱导内质网应激反应。

Cell Stress Chaperones. 2008 Dec;13(4):421-34. doi: 10.1007/s12192-008-0038-0. Epub 2008 Apr 17.

Hematopoietic chimerism and central tolerance created by peripheral-tolerance induction without myeloablative conditioning.通过非清髓性预处理诱导外周耐受所产生的造血嵌合和中枢耐受。

J Clin Invest. 2003 Sep;112(5):795-808. doi: 10.1172/JCI18599.

Skin allograft maintenance in a new synchimeric model system of tolerance.在一种新的同步嵌合耐受模型系统中维持同种异体皮肤移植。

J Immunol. 2001 Dec 1;167(11):6623-30. doi: 10.4049/jimmunol.167.11.6623.

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