Huang L, Sye K, Crispe I N
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06511.
Int Immunol. 1994 Apr;6(4):533-40. doi: 10.1093/intimm/6.4.533.
Small numbers of T cells have been isolated from the normal mouse liver and many of these are of the CD4-CD8-TCR alpha beta+ phenotype. Larger numbers of such cells are present in the livers of mice homozygous for the lpr mutation and the liver has been proposed to be the site of an extrathymic T cell development pathway that is expanded in lpr/lpr mice. Using a modified separation procedure that increases the liver T cell yield, we have been able to characterize a subset of CD4-CD8-TCR alpha beta intermediate T cells that express the B220 epitope of the CD45 molecule, and resemble in this and many other ways the accumulating T cells in lpr lymph nodes. These cells are an actively dividing population and even in healthy, unmanipulated mice a large proportion of them are undergoing apoptosis. We propose the model that the normal liver is a major site for T cell destruction and that the lpr defect results in failure of this process with leakage of B220+CD4-CD8-TCR alpha beta+ cells from the liver to peripheral lymphoid tissues, particularly lymph nodes.
已从小鼠正常肝脏中分离出少量T细胞，其中许多细胞具有CD4-CD8-TCRαβ+表型。在纯合lpr突变的小鼠肝脏中存在大量此类细胞，并且有人提出肝脏是胸腺外T细胞发育途径的场所，在lpr/lpr小鼠中该途径会扩大。使用改良的分离程序提高肝脏T细胞产量后，我们得以鉴定出表达CD45分子B220表位的CD4-CD8-TCRαβ中间型T细胞亚群，这些细胞在这方面以及许多其他方面与lpr淋巴结中积累的T细胞相似。这些细胞是一个活跃分裂的群体，即使在健康、未受操作的小鼠中，其中很大一部分也在经历凋亡。我们提出这样一个模型，即正常肝脏是T细胞破坏的主要场所，而lpr缺陷导致该过程失败，使得B220+CD4-CD8-TCRαβ+细胞从肝脏泄漏到外周淋巴组织，尤其是淋巴结。
