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本文引用的文献

1
Macrophage-mediated suppression. I. Evidence for participation of both hdyrogen peroxide and prostaglandins in suppression of murine lymphocyte proliferation.巨噬细胞介导的抑制作用。I. 过氧化氢和前列腺素参与抑制小鼠淋巴细胞增殖的证据。
J Immunol. 1980 Feb;124(2):983-8.
2
Immune suppression induced by Actinobacillus actinomycetemcomitans. I. Effects on human peripheral blood lymphocyte responses to mitogens and antigens.伴放线放线杆菌诱导的免疫抑制。I. 对人外周血淋巴细胞对丝裂原和抗原反应的影响。
J Immunol. 1982 Jan;128(1):148-54.
3
Suppression of human peripheral blood lymphocytes by Fusobacterium nucleatum.具核梭杆菌对人外周血淋巴细胞的抑制作用
J Immunol. 1984 May;132(5):2357-62.
4
Suppression of human lymphocyte responses by oral spirochetes: a monocyte-dependent phenomenon.口腔螺旋体对人淋巴细胞反应的抑制作用:一种单核细胞依赖现象。
J Immunol. 1984 Apr;132(4):2039-45.
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Interaction of bacteria with the immune system.细菌与免疫系统的相互作用。
J Clin Lab Immunol. 1983 Jan;10(1):1-12.
6
In vivo responses to inhaled proteins. III. Inhibition of experimental immune complex pneumonitis after suppression of peripheral blood lymphocytes.对吸入蛋白的体内反应。III. 外周血淋巴细胞受抑制后实验性免疫复合物肺炎的抑制作用
J Immunol. 1980 Apr;124(4):1763-72.
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Abnormalities of in vitro lymphocyte responses during rubella virus infections.风疹病毒感染期间体外淋巴细胞反应的异常情况。
J Exp Med. 1968 Jul 1;128(1):47-68. doi: 10.1084/jem.128.1.47.
8
A non-specific inhibitor produced by Candida albicans activated T cells impairs cell proliferation by inhibiting interleukin-1 production.白色念珠菌激活的T细胞产生的一种非特异性抑制剂通过抑制白细胞介素-1的产生来损害细胞增殖。
Clin Exp Immunol. 1985 May;60(2):303-10.
9
Immunosuppressive effects of Centipeda periodontii: selective cytotoxicity for lymphocytes and monocytes.石胡荽的免疫抑制作用:对淋巴细胞和单核细胞的选择性细胞毒性。
Infect Immun. 1987 Oct;55(10):2332-40. doi: 10.1128/iai.55.10.2332-2340.1987.
10
Parasite accessory cell interactions in murine leishmaniasis. I. Evasion and stimulus-dependent suppression of the macrophage interleukin 1 response by Leishmania donovani.鼠利什曼病中寄生虫与辅助细胞的相互作用。I. 杜氏利什曼原虫对巨噬细胞白细胞介素1应答的逃避及刺激依赖性抑制
J Immunol. 1987 Mar 15;138(6):1919-25.

中间普氏菌对体外人淋巴细胞活化的免疫抑制作用。

Immunosuppressive effects of Prevotella intermedia on in vitro human lymphocyte activation.

作者信息

Shenker B J, Vitale L, Slots J

机构信息

Department of Pathology, University of Pennsylvania, School of Dental Medicine, Philadelphia 19104-6002.

出版信息

Infect Immun. 1991 Dec;59(12):4583-9. doi: 10.1128/iai.59.12.4583-4589.1991.

DOI:10.1128/iai.59.12.4583-4589.1991
PMID:1937818
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC259081/
Abstract

In this study, we have assessed four strains of Prevotella intermedia, isolated from periodontally involved lesions, for their ability to inhibit lymphocyte functions. All four strains were found to cause a dose-dependent inhibition of B- and T-cell proliferation in response to mitogens and antigens. This was reflected in altered DNA, RNA, and protein syntheses. Furthermore, P. intermedia appeared to affect the early stages of cell activation. This was ascertained by kinetic analysis in which it was determined that the extract had to be present during the first 24 h of incubation to cause suppression. Moreover, direct assessment of the early stages of cell activation indicated that release of cytokines and expression of the interleukin 2 receptor and CD69 on T cells were inhibited by P. intermedia sonic extracts. Finally, preliminary characterization of the immunosuppressive agent indicates that it has a molecular mass of approximately 50 kDa and is heat labile. It has been proposed that impaired host defense may play a pivotal role in the pathogenesis of many infections. The data presented in this paper suggest that microbially mediated immunosuppression may contribute to the pathogenesis of periodontal disease by altering the nature and consequences of host-parasite interactions.

摘要

在本研究中,我们评估了从牙周病变部位分离出的4株中间普氏菌抑制淋巴细胞功能的能力。发现所有4株菌对丝裂原和抗原诱导的B细胞和T细胞增殖均有剂量依赖性抑制作用。这反映在DNA、RNA和蛋白质合成的改变上。此外,中间普氏菌似乎影响细胞活化的早期阶段。这通过动力学分析得以确定,即提取物必须在孵育的最初24小时内存在才能产生抑制作用。此外,对细胞活化早期阶段的直接评估表明,中间普氏菌超声提取物可抑制细胞因子的释放以及T细胞上白细胞介素2受体和CD69的表达。最后,对免疫抑制剂的初步特性分析表明,其分子量约为50 kDa,且对热不稳定。有人提出,宿主防御功能受损可能在许多感染的发病机制中起关键作用。本文提供的数据表明,微生物介导的免疫抑制可能通过改变宿主-病原体相互作用的性质和结果,从而在牙周病的发病机制中发挥作用。