John Beena, Crispe Ian Nicholas
David H. Smith Center for Vaccine Biology and Immunology, Aab Institute for Biomedical Sciences, University of Rochester Medical Center, Rochester, NY 14642, USA.
J Immunol. 2004 May 1;172(9):5222-9. doi: 10.4049/jimmunol.172.9.5222.
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.
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。