Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors.

R H See; A W Chow

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Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors.

机译：蛋白激酶抑制剂可差异抑制葡萄球菌中毒性休克综合征毒素1诱导的人外周血单核细胞和T淋巴细胞分泌的肿瘤坏死因子α和白介素1β。

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The signal transduction pathways by which staphylococcal toxic shock syndrome toxin 1 (TSST-1) induces tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) secretion were examined with various protein kinase inhibitors. TNF-alpha secretion by normal human monocytes and T cells in response to TSST-1 was suppressed by inhibitors of protein kinase C (H7) and tyrosine kinases (genistein). In contrast, the secretion of IL-1 beta was blocked by a cyclic AMP- and cyclic GMP-dependent kinase inhibitor (HA1004) as well as by H7 and genistein. These results suggest that the secretion of TNF-alpha and IL-1 beta may be differentially regulated by TSST-1 and that protein kinases play an important role in mediating cytokine responses to the toxin.

机译：用各种蛋白激酶抑制剂研究了葡萄球菌中毒性休克综合征毒素1（TSST-1）诱导肿瘤坏死因子α（TNF-alpha）和白介素1β（IL-1 beta）分泌的信号转导途径。正常人单核细胞和T细胞对TSST-1的TNF-α分泌受到蛋白激酶C（H7）和酪氨酸激酶（染料木黄酮）抑制剂的抑制。相反，IL-1β的分泌被环状AMP和环状GMP依赖性激酶抑制剂（HA1004）以及H7和染料木黄酮阻断。这些结果表明，TNF-α和IL-1β的分泌可能受到TSST-1的差异调节，并且蛋白激酶在介导对毒素的细胞因子应答中起重要作用。

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《Infection and immunity》 |1992年第8期|共4页
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R H See; A W Chow;
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中图分类医学免疫学;
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1. Role of the adhesion molecule lymphocyte function associated antigen 1 in toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human monocytes. [J] . R H See, A W Chow Infection and immunity . 1992,第11期

机译：粘附分子淋巴细胞功能相关抗原1在中毒性休克综合征毒素1诱导的人类单核细胞分泌的肿瘤坏死因子α和白介素1β的作用。
2. Induction of tumor necrosis factor and interleukin-1 by purified staphylococcal toxic shock syndrome toxin 1 requires the presence of both monocytes and T lymphocytes. [J] . R H See, W W Kum, A H Chang, Infection and immunity . 1992,第7期

机译：通过纯化的葡萄球菌中毒性休克综合征毒素1诱导肿瘤坏死因子和白介素-1要求同时存在单核细胞和T淋巴细胞。
3. Production of Tumor Necrosis Factor Alpha in Human T Lymphocytes by Staphylococcal Enterotoxin B Correlates with Toxin-Induced Proliferation and Is Regulated through Protein Kinase C [J] . Zhengyin Yan, David C. H. Yang, Roger Neill, Infection and immunity . 1999,第12期

机译：葡萄球菌肠毒素B在人T淋巴细胞中产生的肿瘤坏死因子α与毒素诱导的增殖相关，并通过蛋白激酶C调节。
4. Role of Sphingosine Kinase in the Expression of Adhesion Molecules on Monocytes Induced by Tumor Necrosis Factor-Alpha (Relevant to Atherosclerosis) [C] . Tuang Chew Yan, Zhong Liang, Alirio, . 2005

机译：鞘氨醇激酶在肿瘤坏死因子-α（与动脉粥样硬化有关）诱导的单核细胞粘附分子表达中的作用
5. The regulation of the monocyte chemoattractant protein-1 by tumor necrosis factor-alpha requires activation of transcription factors, chromatin modification, and long distance protein-protein communication. [D] . Boekhoudt, Gunther Heinrich. 2003

机译：肿瘤坏死因子-α对单核细胞趋化蛋白-1的调节需要激活转录因子，染色质修饰和长距离蛋白-蛋白通讯。
6. Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors. [O] . R H See, A W Chow 1992

机译：蛋白激酶抑制剂可不同程度抑制人外周血单核细胞和T淋巴细胞分泌的葡萄球菌中毒性休克综合征毒素1诱导的肿瘤坏死因子α和白介素1β分泌。
7. Role of the adhesion molecule lymphocyte function associated antigen 1 in toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human monocytes [O] . R H See, A W Chow 1992

机译：粘附分子淋巴细胞功能相关的抗原1中毒患有毒性休克综合征毒素1诱导肿瘤坏死因子α和白细胞上的白细胞介素-1β分泌

Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors.

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