Divergence between cytotoxic effector function and tumor necrosis factor alpha production for inflammatory CD4+ T cells from mice with Sendai virus pneumonia.
Divergence between cytotoxic effector function and tumor necrosis factor alpha production for inflammatory CD4+ T cells from mice with Sendai virus pneumonia.
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仙台病毒肺炎小鼠炎症 CD4 T 细胞的细胞毒性效应器功能和肿瘤坏死因子 α 产生之间的差异。
DOI：
10.1128/jvi.67.10.6299-6302.1993
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发表时间：
1993
影响因子：
5.4
通讯作者：
Doherty,PC
中科院分区：
文献类型：
--
作者：
Hou,S;Fishman,M;Murti,KG;Doherty,PC
缺乏 CD8+ T 细胞的 β2-微球蛋白缺陷型 [β2-m(-/-)] 小鼠中的仙台病毒肺炎的特征是产生可直接从呼吸道回收的 CD4+ 细胞毒性 T 淋巴细胞。尽管来自 β 2-m (-/-) 和 β 2-m (+/+) 小鼠的炎性 CD4+ T 细胞产生大量肿瘤坏死因子 α，但在 β 2-m (+/+) 小鼠中未发现这些 CD4+ 细胞毒性 T 淋巴细胞。使用也抑制肿瘤坏死因子β的单克隆抗体进行的阻断实验表明，这两种细胞因子的分泌形式并不负责病毒特异性杀死II类主要组织相容性复合体相容性靶标。电子显微照片的比较表明，β 2-m (-/-) 小鼠的 CD4+ 效应子是细胞凋亡的有效诱导剂，而 β 2-m (+/+) CD4+ 组的情况并非如此。这些实验进一步定义了在存在或不存在 CD8+ 效应子的情况下体内响应的病毒特异性 CD4+ T 细胞的功能状态。
Sendai virus pneumonia in beta 2-microglobulin-deficient [beta 2-m(-/-)] mice lacking CD8+ T cells is characterized by the development of CD4+ cytotoxic T lymphocytes that can be recovered directly from the respiratory tract. These CD4+ cytotoxic T lymphocytes are not found in beta 2-m (+/+) mice, though inflammatory CD4+ T cells from both beta 2-m (-/-) and beta 2-m (+/+) mice produce substantial amounts of tumor necrosis factor alpha. Blocking experiments with a monoclonal antibody that also inhibits tumor necrosis factor beta show that the secreted forms of these two cytokines are not responsible for virus-specific killing of class II major histocompatibility complex-compatible targets. Comparison of electron micrographs indicates that the CD4+ effectors from the beta 2-m (-/-) mice are potent inducers of apoptosis, while this is not the case for the beta 2-m (+/+) CD4+ set. These experiments further define the functional status of virus-specific CD4+ T cells responding in vivo in the presence or absence of CD8+ effectors.