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β2-微球蛋白缺陷小鼠表现出针对流感致敏的自体脾细胞的II类主要组织相容性复合体(MHC)限制的抗病毒CD4 + 细胞毒性T淋巴细胞(CTL),但不表现出CD8 + CTL。

Beta 2-microglobulin-deficient mice demonstrate class II MHC restricted anti-viral CD4+ but not CD8+ CTL against influenza-sensitized autologous splenocytes.

作者信息

Taylor S F, Bender B S

机构信息

Department of Veterans Affairs Medical Center, University of Florida College of Medicine, Gainesville 32608, USA.

出版信息

Immunol Lett. 1995 May;46(1-2):67-73. doi: 10.1016/0165-2478(95)00024-y.

DOI:10.1016/0165-2478(95)00024-y
PMID:7590931
Abstract

Mice transgenic for beta 2-microglobulin gene deletion (beta 2M-/-) can clear respiratory pathogens but at a slower rate than control mice. How these mice eliminate virus is not known, but the process is believed to involve CD4+ T cells. Recent studies from other laboratories have suggested a role for CD8+ cytotoxic T lymphocytes (CTLs) in both recognition of beta 2M deficient cells by allogeneic mice and rejection of MHC-incompatible tumor cells by beta 2M-/- mice. After influenza inoculation, we found no evidence for anti-influenza CD8 CTL activity from the lungs or spleens of beta 2M-/- mice. Anti-influenza CD4+, class-II restricted CTL activity was demonstrated from both the lungs and spleens. We next used mitogen-stimulated splenocytes from beta 2M-/- mice for targets in an in vitro CTL assay. This method for determining MHC class II CTL activity showed that the lungs and spleens of influenza-infected beta 2M-/- mice contained precursors to CD4+, but not CD8+, effector CTLs. The data indicate that CD8+ CTLs have no role in anti-viral activity in beta 2M-/- mice. Development of anti-tumor CTLs and anti-viral CTLs may arise via different mechanisms.

摘要

β2-微球蛋白基因缺失的转基因小鼠(β2M-/-)能够清除呼吸道病原体,但清除速度比对照小鼠慢。这些小鼠如何清除病毒尚不清楚,但据信该过程涉及CD4+T细胞。其他实验室最近的研究表明,CD8+细胞毒性T淋巴细胞(CTL)在同种异体小鼠识别β2M缺陷细胞以及β2M-/-小鼠排斥MHC不相容肿瘤细胞中发挥作用。接种流感病毒后,我们未发现β2M-/-小鼠的肺或脾中有抗流感CD8CTL活性的证据。肺和脾中均显示出抗流感CD4+、II类限制性CTL活性。接下来,我们将β2M-/-小鼠经丝裂原刺激的脾细胞用作体外CTL试验的靶细胞。这种确定MHC II类CTL活性的方法表明,感染流感的β2M-/-小鼠的肺和脾中含有CD4+效应CTL的前体细胞,但不含有CD8+效应CTL的前体细胞。数据表明,CD8+CTL在β2M-/-小鼠的抗病毒活性中不起作用。抗肿瘤CTL和抗病毒CTL的发育可能通过不同机制产生。

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