The axis of interleukin 12 and gamma interferon regulates acute vascular xenogeneic rejection

被引：59

作者：

Wang, H

DeVries, ME

Deng, SP

Khandaker, MH

Pickering, JG

Chow, LH

Garcia, B

Kelvin, DJ

Zhong, R

机构：

[1] London Hlth Sci Ctr, Multi Organ Transplant Program, London, ON N6A 5A5, Canada

[2] John P Robarts Res Inst, Expt Transplantat Surg Lab, London, ON N6G 2V4, Canada

[3] Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 5C1, Canada

[4] John P Robarts Res Inst, Lab Mol Immunol & Inflammat, London, ON N6G 2V4, Canada

来源：

NATURE MEDICINE | 2000年 / 6卷 / 05期

关键词：

D O I：

10.1038/75029

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent advances using transgenic animals or exogenous complement inhibitors have demonstrated prevention of hyperacute rejection of vascularized organs, but not graft loss due to acute vascular rejection. Using various wild-type and cytokine-deficient mice strains, we have examined the mechanisms of acute vascular rejection. C57BL/6 mice deficient in interleukin12 or gamma interferon showed faster acute vascular rejection than did wild-type mice. Furthermore, mice defective in B-cell development showed no acute vascular rejection. These results demonstrate that the axis of interleukin 12 and gamma interferon provides a survival advantage in vascularized xenografts by delaying or preventing acute vascular rejection caused by a B cell-dependent mechanism.

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收藏

页码：549 / 555

页数：7

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