Wei W Z, Wang H, Ficsor-Jacobs R, Pauley R
E. Walter Albachten Department of Immunology, Michigan Cancer Foundation, Detroit 48201.
Cancer Res. 1992 Oct 1;52(19):5183-9.
Selective deletion of mature peripheral V beta 2+ T-cells was observed in BALB/c mice implanted with the syngeneic C4 preneoplastic hyperplastic alveolar nodule (HAN) but not in mice with sham surgery (W. Z. Wei, R. Ficsor-Jacobs, S. J. Tsai, and R. Pauley, Cancer Res., 51:3331-3333, 1991). We now report the participation of host cells in that process. Peripheral V beta 2+ T-cells were reduced by 50% or more 4 weeks after an i.v. injection of 10 x 10(6) spleen cells from C4 HAN-bearing mice. Both T- and B-cell-enriched splenocytes mediated V beta 2 deletion. Secondary adoptive transfer of splenocytes from the recipients of the primary adoptive transfer also resulted in V beta 2+ T-cell deletion. The splenocytes lose V beta 2-deleting activity after 500 rad irradiation. V beta 2 deletion induced by either C4 HAN or splenocytes was more profound in CD4+ than in CD8+ T-cells. Loss of V beta 2+CD4+ T-cells was observed 5 days after the adoptive transfer of splenocytes, whereas V beta 2+ CD8+ cells were not reduced until day 9 or later. The differential rate of V beta 2+ CD4+ and CD8+ T-cell reduction continued for at least 7 weeks after the adoptive transfer. The pattern of V beta 2 deletion and the sequence of T-cell loss is similar in the recipients of C4 HAN or of adoptively transferred splenocytes. Southern blot analysis demonstrates non-germ line Mtv or MMTV proviral DNA in C4 HAN. Splenocytes of C4 HAN-bearing mice express a higher level of 1.7-kilobase long terminal repeat transcript than normal BALB/c splenocytes, suggesting a role for a unique Mtv/MMTV provirus in V beta 2 deletion.
在植入同基因C4癌前增生性肺泡结节(HAN)的BALB/c小鼠中观察到成熟外周Vβ2 + T细胞的选择性缺失,但在假手术小鼠中未观察到(W.Z. Wei、R. Ficsor-Jacobs、S.J. Tsai和R. Pauley,《癌症研究》,51:3331 - 3333,1991)。我们现在报告宿主细胞参与了该过程。静脉注射来自携带C4 HAN的小鼠的10×10⁶个脾细胞4周后,外周Vβ2 + T细胞减少了50%或更多。富含T细胞和B细胞的脾细胞均介导Vβ2缺失。初次过继转移的受体的脾细胞的二次过继转移也导致Vβ2 + T细胞缺失。脾细胞在500拉德辐射后失去Vβ2缺失活性。C4 HAN或脾细胞诱导的Vβ2缺失在CD4⁺ T细胞中比在CD8⁺ T细胞中更明显。在脾细胞过继转移5天后观察到Vβ2⁺CD4⁺ T细胞的丢失,而Vβ2⁺ CD8⁺细胞直到第9天或更晚才减少。过继转移后,Vβ2⁺ CD4⁺和CD8⁺ T细胞减少的差异率持续至少7周。在接受C4 HAN或过继转移的脾细胞的受体中,Vβ2缺失模式和T细胞丢失顺序相似。Southern印迹分析表明C4 HAN中存在非种系Mtv或MMTV前病毒DNA。携带C4 HAN的小鼠的脾细胞比正常BALB/c脾细胞表达更高水平的1.7千碱基长末端重复转录本,提示一种独特的Mtv/MMTV前病毒在Vβ2缺失中起作用。