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移植物抗宿主反应引起的狼疮样自身抗体形成并不需要B细胞的Lyb-3+5+亚群。

The Lyb-3+5+ subset of B cells is not required for lupus-like autoantibody formation caused by graft-vs-host reaction.

作者信息

Kimura M, Gleichmann E

出版信息

J Immunol. 1985 Dec;135(6):3845-9.

PMID:3877757
Abstract

We asked the question whether or not the Lyb-3+5+ B cell subset, which is lacking in CBA/N immune defective mice, is required for the lupus-like autoantibody formation caused by graft-vs-host reaction (GVHR). (CBA/N X DBA/2)F1 male defective mice injected with DBA/2 T cells produced IgG autoantibodies to the same extent as did nondefective F1 mice suffering from GVHR. Although a very small number of DBA/2 B cells might have contaminated the T cell inocula, it was shown that these were B cells of the defective F1 mice that produced autoantibodies during the GVHR. This was demonstrated by detecting autoantibodies carrying an immunoglobulin allotype of the F1 recipient. Furthermore, the defective F1 male mice injected with CBA/N lymphoid cells, which were lacking Lyb-3+5+ B cells, also produced autoantibodies. Isotype analysis of antinuclear antibodies revealed that some of them belonged to IgG3 isotype. It was concluded that the ontogenically late-appearing B cell subset is not required for GVH autoimmunity.

摘要

我们提出了一个问题,即CBA/N免疫缺陷小鼠中缺乏的Lyb-3+5+B细胞亚群对于移植物抗宿主反应(GVHR)引起的狼疮样自身抗体形成是否是必需的。注射了DBA/2 T细胞的(CBA/N×DBA/2)F1雄性缺陷小鼠产生IgG自身抗体的程度与患有GVHR的非缺陷F1小鼠相同。尽管极少量的DBA/2 B细胞可能污染了T细胞接种物,但结果表明,这些是在GVHR期间产生自身抗体的缺陷F1小鼠的B细胞。通过检测携带F1受体免疫球蛋白同种异型的自身抗体证明了这一点。此外,注射缺乏Lyb-3+5+B细胞的CBA/N淋巴细胞的缺陷F1雄性小鼠也产生了自身抗体。抗核抗体的同种型分析表明,其中一些属于IgG3同种型。得出的结论是,个体发育后期出现的B细胞亚群对于GVH自身免疫不是必需的。

相似文献

1
The Lyb-3+5+ subset of B cells is not required for lupus-like autoantibody formation caused by graft-vs-host reaction.移植物抗宿主反应引起的狼疮样自身抗体形成并不需要B细胞的Lyb-3+5+亚群。
J Immunol. 1985 Dec;135(6):3845-9.
2
Attempts at standardization of lupus-like graft-vs-host disease: inadvertent repopulation by DBA/2 spleen cells of H-2-different nonirradiated F1 mice.狼疮样移植物抗宿主病标准化的尝试:H-2不同的未受照射F1小鼠被DBA/2脾细胞意外重新定植。
J Immunol. 1983 Jun;130(6):2693-701.
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Further evidence against random polyclonal antibody formation in mice with lupus-like graft-vs-host disease.反对患有狼疮样移植物抗宿主病的小鼠中随机多克隆抗体形成的进一步证据。
J Immunol. 1984 Apr;132(4):1814-20.
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Selective production of autoantibodies in graft-vs-host-induced and spontaneous murine lupus. Predominant reactivity with histone regions accessible in chromatin.移植物抗宿主诱导的和自发性小鼠狼疮中自身抗体的选择性产生。与染色质中可及的组蛋白区域具有主要反应性。
J Immunol. 1988 Feb 1;140(3):755-60.
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The asymmetry in idiotype-isotype expression in the response to phosphocholine is due to divergence in the expressed repertoires of Lyb-5+ and Lyb-5- B cells.对磷酸胆碱反应中独特型-同种型表达的不对称性是由于Lyb-5+和Lyb-5- B细胞表达库的差异所致。
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Polyclonal B cell activation by a B cell differentiation factor, B151-TRF2. III. B151-TRF2 as a B cell differentiation factor closely associated with autoimmune disease.B细胞分化因子B151-TRF2引起的多克隆B细胞活化。III. B151-TRF2作为一种与自身免疫性疾病密切相关的B细胞分化因子。
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T-B collaboration for autoantibody production in lpr mice is cognate and MHC-restricted.lpr小鼠中T细胞与B细胞协作产生自身抗体是同源且受主要组织相容性复合体(MHC)限制的。
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Contribution of Lyb 5+ and Lyb 5- B cells to the primary and secondary phosphocholine-specific antibody response.Lyb 5+和Lyb 5- B细胞对初次和二次磷酸胆碱特异性抗体反应的贡献。
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Diseases caused by reactions of T lymphocytes to incompatible structures of the major histocompatibility complex. V. High titers of IgG autoantibodies to double-stranded DNA.由T淋巴细胞对主要组织相容性复合体不相容结构的反应所引起的疾病。五、针对双链DNA的高滴度IgG自身抗体。
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In vivo allogeneic effects: shift in the isotype profile of primary TI-2 responses in mice undergoing graft-vs-host reaction.体内同种异体效应:在发生移植物抗宿主反应的小鼠中,原发性TI-2反应的免疫球蛋白同种型谱发生改变。
J Immunol. 1982 Nov;129(5):1878-82.

引用本文的文献

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Mechanisms of physiologic B cell responses and B cell hyperactivity in systemic lupus erythematosus.系统性红斑狼疮中生理性B细胞反应及B细胞功能亢进的机制
Springer Semin Immunopathol. 1986;9(2-3):195-218. doi: 10.1007/BF02099022.