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与小鼠宿主抗移植物病相关的自身免疫性疾病和恶性淋巴瘤。

Autoimmune disease and malignant lymphoma associated with host-versus-graft disease in mice.

作者信息

Tateno M, Kondo N, Itoh T, Yoshiki T

出版信息

Clin Exp Immunol. 1985 Dec;62(3):535-44.

PMID:4085149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1577477/
Abstract

BALB/c mice neonatally injected with (BALB/c X C57BL/6)F1 hybrid spleen cells develop host-versus-graft disease (HVGD) with immunopathological features characteristic of either systemic lupus erythematosus (SLE), or immunoblastic lymphadenopathy (IBL) in man. HVGD mice manifest polyclonal hypergammaglobulinemia with various autoantibodies, generalized lymphadenopathy, hepatosplenomegaly, immune complex glomerulonephritis and evolve in the end to malignant lymphoma. The necessary prerequisite for HVGD induction between donor and host can be summarized as follows: Histoincompatibilities in the H-2 region between donor and host are needed; predominant F1 donor cells needed for HVGD induction are, if not sole, steroid resistant, nylon wool nonadherent and Thy-1 positive T cells; the role of donor T cells is not only to present H-2 complex to the host, but also to interact with and proliferate in the host; strain differences are found for the susceptibility of HVGD induction in the host. It has been found that HVGD evolves to a malignant lymphoma of host T cell origin. The HVGD mouse model may, therefore, contribute to the understanding of the cell to cell interactions at work in the pathogenesis of IBL, as well as SLE, in man.

摘要

新生期注射(BALB/c×C57BL/6)F1杂交脾细胞的BALB/c小鼠会发生宿主抗移植物病(HVGD),其免疫病理学特征与人类系统性红斑狼疮(SLE)或免疫母细胞性淋巴结病(IBL)的特征相似。HVGD小鼠表现出多克隆高丙种球蛋白血症并伴有多种自身抗体、全身性淋巴结病、肝脾肿大、免疫复合物性肾小球肾炎,最终发展为恶性淋巴瘤。供体与宿主之间诱导HVGD的必要前提可总结如下:供体与宿主之间的H-2区域存在组织不相容性;诱导HVGD所需的主要F1供体细胞(若不是唯一的)是对类固醇耐药、不黏附尼龙毛且Thy-1阳性的T细胞;供体T细胞的作用不仅是向宿主呈递H-2复合体,还与宿主相互作用并在宿主体内增殖;宿主对HVGD诱导的易感性存在品系差异。已发现HVGD会发展为宿主T细胞来源的恶性淋巴瘤。因此,HVGD小鼠模型可能有助于理解在人类IBL以及SLE发病机制中起作用的细胞间相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ba/1577477/7e03a5f50c4a/clinexpimmunol00129-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ba/1577477/f1ab70fabbbd/clinexpimmunol00129-0091-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ba/1577477/7e03a5f50c4a/clinexpimmunol00129-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ba/1577477/f1ab70fabbbd/clinexpimmunol00129-0091-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33ba/1577477/7e03a5f50c4a/clinexpimmunol00129-0095-a.jpg

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本文引用的文献

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Unfractionated spleen cells but not natural killer (NK) cells from RFM donors prevent the progression of host-versus-graft disease in murine RFM/(T6 x RFM)F1 chimeras.来自辐射嵌合体小鼠(RFM)供体的未分级脾细胞而非自然杀伤(NK)细胞,可阻止宿主抗移植物疾病在鼠RFM/(T6×RFM)F1嵌合体中的进展。
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