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被动和主动机制将活化的CD8 + T细胞捕获在肝脏中。

Passive and active mechanisms trap activated CD8+ T cells in the liver.

作者信息

John Beena, Crispe Ian Nicholas

机构信息

David H. Smith Center for Vaccine Biology and Immunology, Aab Institute for Biomedical Sciences, University of Rochester Medical Center, Rochester, NY 14642, USA.

出版信息

J Immunol. 2004 May 1;172(9):5222-9. doi: 10.4049/jimmunol.172.9.5222.

Abstract

The liver is a site where activated CD8(+) T cells are trapped and destroyed at the end of an immune response. The intrahepatic accumulation of activated murine TCR transgenic CD8(+) T cells was significantly reduced when either ICAM-1 or VCAM-1 was blocked by specific Ab. These two adhesion mechanisms account for essentially all the trapping of activated CD8(+) T cells in the mouse liver. Although the ICAM-1-mediated trapping depends on the capacity of the vasculature and/or the parenchymal cells to present Ag, the accumulation of cells through VCAM-1 does not require Ag recognition. Thus, Ags expressed by the non-bone marrow-derived cells in the liver actively cause CD8(+) T cell accumulation through TCR-activated ICAM-1 adhesion, but the liver can also passively sequester activated CD8(+) T cells that do not recognize intrahepatic Ag, through VCAM-1 adhesion.

摘要

肝脏是免疫反应末期活化的CD8(+) T细胞被捕获并被清除的场所。当ICAM-1或VCAM-1被特异性抗体阻断时,活化的小鼠TCR转基因CD8(+) T细胞在肝内的蓄积显著减少。这两种黏附机制基本上解释了活化的CD8(+) T细胞在小鼠肝脏中的所有捕获情况。虽然ICAM-1介导的捕获依赖于脉管系统和/或实质细胞呈递抗原的能力,但通过VCAM-1的细胞蓄积并不需要抗原识别。因此,肝脏中非骨髓来源细胞表达的抗原通过TCR激活的ICAM-1黏附作用积极地导致CD8(+) T细胞蓄积,但肝脏也可以通过VCAM-1黏附被动隔离不识别肝内抗原的活化CD8(+) T细胞。

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