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The effect of site-specific monoclonal antibodies directed to toxic shock syndrome toxin-1 in experimental Staphylococcus aureus arthritis.针对中毒性休克综合征毒素-1的位点特异性单克隆抗体在实验性金黄色葡萄球菌关节炎中的作用。
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Delineation by use of specific monoclonal antibodies of the T-cell receptor and major histocompatibility complex interaction sites on the superantigen toxic shock syndrome toxin 1.利用特异性单克隆抗体描绘超抗原中毒性休克综合征毒素1上的T细胞受体与主要组织相容性复合体相互作用位点。
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V beta 11+ T-lymphocyte expansion by toxic shock syndrome toxin-1 differs in mice bearing H-2q versus H-2b haplotypes.中毒性休克综合征毒素-1引起的Vβ11 + T淋巴细胞扩增在携带H-2q与H-2b单倍型的小鼠中存在差异。
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Clonal expansion of T lymphocytes causes arthritis and mortality in mice infected with toxic shock syndrome toxin-1-producing staphylococci.T淋巴细胞的克隆性扩增会导致感染产生中毒性休克综合征毒素-1的葡萄球菌的小鼠出现关节炎和死亡。
Eur J Immunol. 1994 May;24(5):1161-6. doi: 10.1002/eji.1830240523.
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Toxic shock syndrome toxin-1-induced death is prevented by CTLA4Ig.细胞毒性T淋巴细胞相关抗原4免疫球蛋白(CTLA4Ig)可预防中毒性休克综合征毒素-1诱导的死亡。
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Defining a novel domain of staphylococcal toxic shock syndrome toxin-1 critical for major histocompatibility complex class II binding, superantigenic activity, and lethality.确定葡萄球菌中毒性休克综合征毒素-1的一个新结构域,该结构域对主要组织相容性复合体II类结合、超抗原活性和致死性至关重要。
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Functional analysis of the TCR binding domain of toxic shock syndrome toxin-1 predicts further diversity in MHC class II/superantigen/TCR ternary complexes.中毒性休克综合征毒素-1的TCR结合域功能分析预示着MHC II类/超抗原/TCR三元复合物中存在更多样性。
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Structural basis for differential binding of staphylococcal enterotoxin A and toxic shock syndrome toxin 1 to class II major histocompatibility molecules.葡萄球菌肠毒素A和中毒性休克综合征毒素1与II类主要组织相容性分子差异结合的结构基础。
Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):125-8. doi: 10.1073/pnas.88.1.125.

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Identification of a novel fully human anti-toxic shock syndrome toxin (TSST)-1 single-chain variable fragment antibody averting TSST-1-induced mitogenesis and cytokine secretion.鉴定一种新型的完全人源抗中毒性休克综合征毒素(TSST-1)单链可变片段抗体,可避免 TSST-1 诱导的有丝分裂和细胞因子分泌。
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本文引用的文献

1
Defining a novel domain of staphylococcal toxic shock syndrome toxin-1 critical for major histocompatibility complex class II binding, superantigenic activity, and lethality.确定葡萄球菌中毒性休克综合征毒素-1的一个新结构域,该结构域对主要组织相容性复合体II类结合、超抗原活性和致死性至关重要。
Can J Microbiol. 2000 Feb;46(2):171-9.
2
Arthritis and sepsis caused by Staphylococcus aureus: can the tissue injury be reduced by modulating the host's immune system?金黄色葡萄球菌引起的关节炎和败血症:能否通过调节宿主免疫系统来减轻组织损伤?
Mol Med Today. 1998 Jan;4(1):15-8. doi: 10.1016/S1357-4310(97)80540-0.
3
Differential effects of staphylococcal toxic shock syndrome toxin-1 on B cell apoptosis.葡萄球菌中毒性休克综合征毒素-1对B细胞凋亡的不同影响。
Proc Natl Acad Sci U S A. 1996 May 28;93(11):5425-30. doi: 10.1073/pnas.93.11.5425.
4
Delineation by use of specific monoclonal antibodies of the T-cell receptor and major histocompatibility complex interaction sites on the superantigen toxic shock syndrome toxin 1.利用特异性单克隆抗体描绘超抗原中毒性休克综合征毒素1上的T细胞受体与主要组织相容性复合体相互作用位点。
Infect Immun. 1996 Apr;64(4):1133-9. doi: 10.1128/iai.64.4.1133-1139.1996.
5
The accessory gene regulator (agr) controls Staphylococcus aureus virulence in a murine arthritis model.辅助基因调节因子(agr)在小鼠关节炎模型中控制金黄色葡萄球菌的毒力。
Infect Immun. 1993 Sep;61(9):3879-85. doi: 10.1128/iai.61.9.3879-3885.1993.
6
Structure of toxic shock syndrome toxin 1.中毒性休克综合征毒素1的结构
Biochemistry. 1993 Dec 21;32(50):13761-6. doi: 10.1021/bi00213a001.
7
Clonal expansion of T lymphocytes causes arthritis and mortality in mice infected with toxic shock syndrome toxin-1-producing staphylococci.T淋巴细胞的克隆性扩增会导致感染产生中毒性休克综合征毒素-1的葡萄球菌的小鼠出现关节炎和死亡。
Eur J Immunol. 1994 May;24(5):1161-6. doi: 10.1002/eji.1830240523.
8
Toxic shock syndrome toxin 1 contributes to the arthritogenicity of Staphylococcus aureus.中毒性休克综合征毒素1促成了金黄色葡萄球菌的致关节炎性。
J Infect Dis. 1994 Jul;170(1):94-9. doi: 10.1093/infdis/170.1.94.
9
Mice with the xid B cell defect are less susceptible to developing Staphylococcus aureus-induced arthritis.患有xid B细胞缺陷的小鼠对金黄色葡萄球菌诱导的关节炎的易感性较低。
J Immunol. 1995 Aug 15;155(4):2067-76.
10
Immunochemical quantitation of antigens by single radial immunodiffusion.通过单向辐射免疫扩散法对抗原进行免疫化学定量。
Immunochemistry. 1965 Sep;2(3):235-54. doi: 10.1016/0019-2791(65)90004-2.

针对中毒性休克综合征毒素-1的位点特异性单克隆抗体在实验性金黄色葡萄球菌关节炎中的作用。

The effect of site-specific monoclonal antibodies directed to toxic shock syndrome toxin-1 in experimental Staphylococcus aureus arthritis.

作者信息

Verdrengh M, Kum W, Chow A, Tarkowski A

机构信息

Department of Rheumatology, University of Göteborg, Göteborg, Sweden.

出版信息

Clin Exp Immunol. 1999 Nov;118(2):268-70. doi: 10.1046/j.1365-2249.1999.01061.x.

DOI:10.1046/j.1365-2249.1999.01061.x
PMID:10540189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1905427/
Abstract

Staphylococcus aureus produces a large number of potential virulence factors, among these the superantigen toxic shock syndrome toxin-1 (TSST-1). We have recently demonstrated that TSST-1 is involved in the pathogenesis of septic arthritis. Recent data show that the TSST-1 molecule is composed of two distinct domains, one proposed to interact with T cell receptor (TCR) and one with the MHC class II. The aim of this study was to assess if interaction between TSST-1-specific MoAbs directed to sites on the MHC and/or TCR Vbeta affects the development of experimental S. aureus-induced arthritis. For that purpose we used a panel of seven MoAbs, which were injected intraperitoneally before and after inoculation with a TSST-1-producing S. aureus strain. Administration of antibodies did not affect the development of arthritis, suggesting inefficacy of such a procedure in neutralization of exotoxin-mediated disease manifestations.

摘要

金黄色葡萄球菌可产生大量潜在的毒力因子,其中包括超抗原中毒性休克综合征毒素-1(TSST-1)。我们最近证实TSST-1参与了脓毒性关节炎的发病机制。最近的数据表明,TSST-1分子由两个不同的结构域组成,一个被认为与T细胞受体(TCR)相互作用,另一个与MHC II类分子相互作用。本研究的目的是评估针对MHC和/或TCR Vβ位点的TSST-1特异性单克隆抗体之间的相互作用是否会影响实验性金黄色葡萄球菌诱导的关节炎的发展。为此,我们使用了一组七种单克隆抗体,在接种产生TSST-1的金黄色葡萄球菌菌株之前和之后腹腔注射。抗体的施用并未影响关节炎的发展,这表明该程序在中和外毒素介导的疾病表现方面无效。