ELEVATED-TEMPERATURE REGULATES TUMOR NECROSIS FACTOR-MEDIATED IMMUNE KILLING
ELEVATED-TEMPERATURE REGULATES TUMOR NECROSIS FACTOR-MEDIATED IMMUNE KILLING
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DOI：
10.1002/eji.1830190927
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发表时间：
1989-09-01
影响因子：
5.4
通讯作者：
JANEWAY, CA
中科院分区：
文献类型：
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作者：
GROMKOWSKI, SH;YAGI, JJ;JANEWAY, CA
在体外系统中研究了高温（热/发热）对炎症过程调节的影响。由于肿瘤坏死因子（TNF），在炎症中的中央介质，是一种热原和细胞因子能够诱导某些细胞的死亡，我们研究了热休克和TNF介导的免疫杀伤之间的关系。WEHI-164纤维肉瘤细胞的热休克显着（和短暂）降低这些细胞的敏感性重组肿瘤坏死因子介导的溶解和II类主要组织相容性复合物特异性，肿瘤坏死因子分泌炎性T细胞介导的溶解。在升高的温度下孵育炎性T淋巴细胞瞬时消除其裂解潜力和分泌TNF的能力。我们的数据表明，TNF的热原活性可以通过诱导靶细胞中保护性蛋白的合成和抑制效应T淋巴细胞分泌TNF来控制炎症期间的细胞溶解过程。
The effect of elevated temperature (heat/fever) on the regulation of inflammatory processes was studied in an in vitro system. Since tumor necrosis factor (TNF), a central mediator in inflammation, is both a pyrogen and a cytokine capable of inducing the death of certain cells, we examined the relationship between heat shock and TNF-mediated immune killing. Heat shock of WEHI-164 fibrosarcoma cells significantly (and transiently) decreased the sensitivity of these cells to recombinant TNF-mediated lysis and to class II major histocompatibility complex-specific, TNF-secreting inflammatory T cell-mediated lysis. Incubating inflammatory T lymphocytes in elevated temperature transiently abolished their lytic potential and their ability to secrete TNF. Our data show that the pyrogen activity of TNF could control cytolytic processes during inflammation both by inducing protective protein(s) synthesis in target cells and by arresting TNF secretion by effector T lymphocytes.