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本文引用的文献

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Immunoregulatory effects of superantigens: interactions of staphylococcal enterotoxins with host MHC and non-MHC products.
Immunol Rev. 1993 Feb;131:27-42. doi: 10.1111/j.1600-065x.1993.tb01528.x.
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Three-dimensional structure of the human class II histocompatibility antigen HLA-DR1.人类II类组织相容性抗原HLA - DR1的三维结构。
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Toxicity of staphylococcal enterotoxins potentiated by lipopolysaccharide: major histocompatibility complex class II molecule dependency and cytokine release.脂多糖增强葡萄球菌肠毒素的毒性:主要组织相容性复合体II类分子依赖性及细胞因子释放
Infect Immun. 1993 Dec;61(12):5333-8. doi: 10.1128/iai.61.12.5333-5338.1993.
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Binary and ternary complexes between T-cell receptor, class II MHC and superantigen in vitro.体外T细胞受体、II类主要组织相容性复合体与超抗原之间的二元和三元复合物
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Class I and class II major histocompatibility molecules play a role in bone marrow-derived macrophage development.I类和II类主要组织相容性分子在骨髓来源的巨噬细胞发育中发挥作用。
J Leukoc Biol. 1994 May;55(5):658-61. doi: 10.1002/jlb.55.5.658.
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Three-dimensional structure of a human class II histocompatibility molecule complexed with superantigen.与超抗原复合的人类II类组织相容性分子的三维结构。
Nature. 1994 Apr 21;368(6473):711-8. doi: 10.1038/368711a0.
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Differential RNA regulation by staphylococcal enterotoxins A and B in murine macrophages.葡萄球菌肠毒素A和B对小鼠巨噬细胞的RNA差异调控
J Leukoc Biol. 1994 Apr;55(4):523-9. doi: 10.1002/jlb.55.4.523.
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Evidence for superantigen involvement in insulin-dependent diabetes mellitus aetiology.超抗原参与胰岛素依赖型糖尿病病因学的证据。
Nature. 1994 Sep 22;371(6495):351-5. doi: 10.1038/371351a0.
9
Binding and activation of major histocompatibility complex class II-deficient macrophages by staphylococcal exotoxins.葡萄球菌外毒素对主要组织相容性复合体II类缺陷巨噬细胞的结合与激活
Infect Immun. 1994 Sep;62(9):3907-15. doi: 10.1128/iai.62.9.3907-3915.1994.
10
Monoclonal antibodies to mouse MHC antigens. III. Hybridoma antibodies reacting to antigens of the H-2b haplotype reveal genetic control of isotype expression.抗小鼠主要组织相容性复合体(MHC)抗原的单克隆抗体。III. 与H-2b单倍型抗原发生反应的杂交瘤抗体揭示了同种型表达的遗传控制。
J Immunol. 1981 Jan;126(1):317-21.

葡萄球菌肠毒素与巨噬细胞上的H-2Db分子结合。

Staphylococcal enterotoxins bind H-2Db molecules on macrophages.

作者信息

Beharka A A, Iandolo J J, Chapes S K

机构信息

Division of Biology, Kansas State University, Manhattan 66506, USA.

出版信息

Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6294-8. doi: 10.1073/pnas.92.14.6294.

DOI:10.1073/pnas.92.14.6294
PMID:7603985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC41504/
Abstract

We screened a panel of monoclonal antibodies against selected macrophage cell surface molecules for their ability to inhibit enterotoxin binding to major histocompatibility complex class II-negative C2D (H-2b) macrophages. Two monoclonal antibodies, HB36 and TIB126, that are specific for the alpha 2 domain of major histocompatibility complex class I, blocked staphylococcal enterotoxins A and B (SEA and SEB, respectively) binding to C2D macrophages in a specific and concentration-dependent manner. Inhibitory activities were haplotype-specific in that SEA and SEB binding to H-2k or H-2d macrophages was not inhibited by either monoclonal antibody. HB36, but not TIB126, inhibited enterotoxin-induced secretion of cytokines by H-2b macrophages. Lastly, passive protection of D-galactosamine-sensitized C2D mice by injection with HB36 antibody prevented SEB-induced death. Therefore, SEA and SEB binding to the alpha 2 domain of the H-2Db molecule induces biological activity and has physiological consequences.

摘要

我们筛选了一组针对特定巨噬细胞表面分子的单克隆抗体,以检测它们抑制肠毒素与主要组织相容性复合体II类阴性C2D(H-2b)巨噬细胞结合的能力。两种对主要组织相容性复合体I类α2结构域具有特异性的单克隆抗体HB36和TIB126,以特异性和浓度依赖性方式阻断葡萄球菌肠毒素A和B(分别为SEA和SEB)与C2D巨噬细胞的结合。抑制活性具有单倍型特异性,即SEA和SEB与H-2k或H-2d巨噬细胞的结合均未被任何一种单克隆抗体抑制。HB36而非TIB126抑制H-2b巨噬细胞肠毒素诱导的细胞因子分泌。最后,通过注射HB36抗体对D-半乳糖胺致敏的C2D小鼠进行被动保护,可预防SEB诱导的死亡。因此,SEA和SEB与H-2Db分子的α2结构域结合可诱导生物活性并产生生理后果。