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首页> 外文期刊>Infection and immunity >Differential induction of tumor necrosis factor alpha in murine and human leukocytes by Mycoplasma arthritidis-derived superantigen.
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Differential induction of tumor necrosis factor alpha in murine and human leukocytes by Mycoplasma arthritidis-derived superantigen.

机译：关节炎支原体来源的超抗原在鼠和人白细胞中差异诱导肿瘤坏死因子α。

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Mycoplasma arthritidis-derived superantigen (MAS) is exclusively produced by M. arthritidis, which is the only known mycoplasma to produce a superantigen. As a superantigen, MAS shows properties similar to those of the staphylococcal enterotoxins and related substances, such as binding to major histocompatibility complex (MHC) class II and V beta-specific stimulation of T cells. In this series of experiments, we demonstrate some differences between MAS and other superantigens. MAS induced the production of tumor necrosis factor alpha (TNF-alpha) mRNA in human as well as in murine leukocytes. However, only in murine leukocytes was the mRNA adequately translated into the protein. In human peripheral blood mononuclear cells, we found only small amounts of TNF, whereas in murine spleen cells we detected levels more than three times higher. The proliferative response to MAS has been shown to be restricted to I-E alpha in the murine MHC. Furthermore, TNF was induced in I-E alpha+ bone marrow-derived macrophages by MAS. In these cells, MAS rapidly induced very high levels of TNF and the amounts of mRNA detected correlated to the amount of protein produced. In comparison with other superantigens, including the staphylococcal enterotoxins, toxic shock syndrome toxin 1, and exfoliative toxin A, the failure of MAS to induce TNF-alpha in human peripheral blood mononuclear cells is specific for MAS and not common to all superantigens. The direct activation of bone marrow-derived macrophages also seems to be specific for MAS. These data suggest that the induction of TNF-alpha by MAS is dependent on the strength of binding to the MHC class II molecule.
机译：关节炎支原体来源的超抗原（MAS）仅由关节炎支原体产生，这是唯一已知的产生超抗原的支原体。作为一种超抗原，MAS显示出与葡萄球菌肠毒素和相关物质相似的特性，例如与主要的组织相容性复合物（MHC）II类和Vβ特异性刺激T细胞结合。在这一系列实验中，我们证明了MAS和其他超抗原之间的一些差异。 MAS诱导人以及鼠白细胞中肿瘤坏死因子α（TNF-alpha）mRNA的产生。但是，只有在鼠白细胞中，mRNA才能充分翻译成蛋白质。在人类外周血单核细胞中，我们仅发现少量的TNF，而在鼠脾细胞中，我们检测到的水平高出三倍以上。在鼠MHC中，已显示对MAS的增殖反应限于I-Eα。此外，通过MAS在I-Eα+骨髓衍生的巨噬细胞中诱导TNF。在这些细胞中，MAS迅速诱导出非常高水平的TNF，并且检测到的mRNA量与产生的蛋白质量相关。与其他超级抗原（包括葡萄球菌肠毒素，中毒性休克综合征毒素1和剥脱性毒素A）相比，MAS在人外周血单核细胞中诱导TNF-α的失败是MAS特有的，并非所有超级抗原都常见。骨髓来源的巨噬细胞的直接激活似乎也对MAS具有特异性。这些数据表明，MAS对TNF-α的诱导取决于与MHC II类分子的结合强度。

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