传播小鼠乳腺肿瘤病毒（MMTV）需要T细胞上的CD40配体与B细胞上的CD40之间的直接物理相互作用。

Direct physical interaction involving CD40 ligand on T cells and CD40 on B cells is required to propagate MMTV.

作者信息

Chervonsky A V, Xu J, Barlow A K, Khery M, Flavell R A, Janeway C A

机构信息

Section of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, New Haven, Connecticut 06510, USA.

出版信息

Immunity. 1995 Jul;3(1):139-46. doi: 10.1016/1074-7613(95)90166-3.

DOI:10.1016/1074-7613(95)90166-3

PMID:7542547

Abstract

The propagation of mouse mammary tumor virus (MMTV) has been analyzed in mice defective for expression of CD40 ligand (CD40L). Mice with endogenous viral superantigen (SAG) delete T cells with cognate V beta independent of CD40L expression. Nevertheless, CD40L-mice do not show deletion of cognate T cells after being exposed to infectious MMTV and have greatly diminished viral replication. The response of CD40L- T cells to SAG in vitro is also impaired, but can be reconstituted by adding B cells activated by recombinant CD40L to express costimulatory molecules. Thus, direct CD40L-dependent B cell activation appears to be a critical step in the life cycle of MMTV. The initial step in SAG-dependent T cell activation, and hence the MMTV life cycle, may be mediated by non-B cells, because splenocytes from B cell-deficient SAG-transgenic mice are able to activate cognate T cells.

摘要

已在缺乏CD40配体（CD40L）表达的小鼠中分析了小鼠乳腺肿瘤病毒（MMTV）的传播情况。携带内源性病毒超抗原（SAG）的小鼠可独立于CD40L表达而删除具有同源Vβ的T细胞。然而，CD40L基因敲除小鼠在接触传染性MMTV后并未出现同源T细胞的缺失，且病毒复制大幅减少。CD40L基因敲除的T细胞在体外对SAG的反应也受损，但通过添加经重组CD40L激活以表达共刺激分子的B细胞可使其恢复。因此，直接的CD40L依赖性B细胞激活似乎是MMTV生命周期中的关键步骤。SAG依赖性T细胞激活的初始步骤以及MMTV的生命周期可能由非B细胞介导，因为来自B细胞缺陷型SAG转基因小鼠的脾细胞能够激活同源T细胞。