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小鼠移植物抗宿主自身免疫中H-2亚区差异的需求:II类H-2抗原(I-A/I-E)差异的优势

Requirement of H-2-subregion differences for graft-versus-host autoimmunity in mice: superiority of the differences at class-II H-2 antigens (I-A/I-E).

作者信息

Kimura M, van Rappard-van der Veen F M, Gleichmann E

出版信息

Clin Exp Immunol. 1986 Sep;65(3):542-52.

PMID:3490938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1542513/
Abstract

The effect of various H-2-subregion differences on graft-versus-host (GVH) autoimmunity in mice was investigated by testing a variety of GVH combinations in which non-irradiated adult F1 hybrid mice were injected with parental strain lymphoid cells. As with previous results, the superiority of Class-II H-2 antigen (I-A/I-E) differences to other kinds of H-2 incompatibilities, such as Class-I H-2 antigen (H-2K/H-2D) differences, was largely confirmed. Anti-nuclear antibodies were produced significantly across Class-I as well as Class-II H-2 differences. However, the productions of anti-erythrocyte and anti-thymocyte autoantibodies were mainly confined to GVH reactions induced across Class-II H-2 antigens. Elevated proteinuria was elicited only in the GVH combinations that included the differences at Class-II H-2 antigens. GVH autoimmunity, however, did not always result in the significant occurrence of elevated proteinuria. The level of in-vitro IgG production by GVH spleen cells correlated closely with the degree of autoimmunity.

摘要

通过检测多种移植物抗宿主(GVH)组合来研究不同H-2亚区差异对小鼠GVH自身免疫的影响,在这些组合中,未受照射的成年F1杂交小鼠被注射亲代品系淋巴细胞。与先前的结果一样,II类H-2抗原(I-A/I-E)差异相对于其他类型的H-2不相容性(如I类H-2抗原(H-2K/H-2D)差异)的优势在很大程度上得到了证实。I类和II类H-2差异均显著产生抗核抗体。然而,抗红细胞和抗胸腺细胞自身抗体的产生主要局限于由II类H-2抗原引发的GVH反应。仅在包含II类H-2抗原差异的GVH组合中引发蛋白尿升高。然而,GVH自身免疫并不总是导致蛋白尿显著升高。GVH脾细胞的体外IgG产生水平与自身免疫程度密切相关。

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Requirement of H-2-subregion differences for graft-versus-host autoimmunity in mice: superiority of the differences at class-II H-2 antigens (I-A/I-E).小鼠移植物抗宿主自身免疫中H-2亚区差异的需求:II类H-2抗原(I-A/I-E)差异的优势
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本文引用的文献

1
A systemic lupus erythematosus (SLE)-like disease in mice induced by abnormal T-B cell cooperation. Preferential formation of autoantibodies characteristic of SLE.由异常T细胞与B细胞协作诱导的小鼠系统性红斑狼疮(SLE)样疾病。优先形成SLE特征性自身抗体。
Eur J Immunol. 1982 Feb;12(2):152-9. doi: 10.1002/eji.1830120210.
2
Diseases caused by reactions of T lymphocytes towards incompatible structures of the major histocompatibility complex. VI. Autoantibodies characteristic of systemic lupus erythematosus induced by abnormal T-B cell cooperation across I-E.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。VI. 跨I-E的异常T-B细胞协作诱导产生的系统性红斑狼疮特征性自身抗体
J Exp Med. 1982 May 1;155(5):1555-60. doi: 10.1084/jem.155.5.1555.
3
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。
J Immunol. 1981 Dec;127(6):2435-8.
4
Diseases caused by reactions of T lymphocytes to incompatible structures of the major histocompatibility complex. III. Autoantibodies to thymocytes.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。III. 针对胸腺细胞的自身抗体。
J Immunol. 1981 Oct;127(4):1281-6.
5
Variable synthesis and expression of E alpha and Ae (E beta) Ia polypeptide chains in mice of different H-2 haplotypes.不同H-2单倍型小鼠中Eα和Ae(Eβ)Ia多肽链的可变合成与表达
Immunogenetics. 1981;12(3-4):321-37. doi: 10.1007/BF01561674.
6
Chromosome 4 Jt gene controls murine T cell surface I-J expression.4号染色体Jt基因控制小鼠T细胞表面I-J的表达。
Science. 1984 Feb 10;223(4636):559-63. doi: 10.1126/science.6607530.
7
Intra-H-2 and T cell requirements for the induction of maximal positive and negative allogeneic effects in vitro.
Eur J Immunol. 1983 Mar;13(3):191-7. doi: 10.1002/eji.1830130303.
8
Capacity of genetically different T lymphocytes to induce lethal graft-versus-host disease correlates with their capacity to generate suppression but not with their capacity to generate anti-F1 killer cells. A non-H-2 locus determines the inability to induce lethal graft-versus-host disease.基因不同的T淋巴细胞诱导致死性移植物抗宿主病的能力与其产生抑制作用的能力相关,而与其产生抗F1杀伤细胞的能力无关。一个非H-2基因座决定了无法诱导致死性移植物抗宿主病。
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9
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J Exp Med. 1983 Aug 1;158(2):546-58. doi: 10.1084/jem.158.2.546.
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J Exp Med. 1983 Feb 1;157(2):755-71. doi: 10.1084/jem.157.2.755.