Suppr超能文献

对鼠逆转录病毒诱导的免疫抑制的抗性的过继转移。

Adoptive transfer of resistance to murine retrovirus-induced immune suppression.

作者信息

Gilmore G L

机构信息

Department of Immunology, Medical Biology Institute, La Jolla, California, USA.

出版信息

Cell Immunol. 1996 Apr 10;169(1):24-9. doi: 10.1006/cimm.1996.0086.

Abstract

Infection of certain strains of mice, such as C57BL/6 and C57BL/10 [B10], with LP-BM5 murine leukemia virus (MuLV) rapidly causes a profound and lethal immune suppression. The H2d congenic strain of B10, B10.D2, is resistant to disease, but B10 x B10.D2 F1 mice are susceptible, indicating that disease sensitivity is dominant. To determine whether disease resistance could be adoptively transferred to a sensitive host, radiation chimeras (B10.D2 --> B10 x B10.D2 F1 and F1 --> F1) were challenged with LP-BM5 virus. Infected B10.D2 --> F1 chimeras showed no loss of immune function, whereas F1 --> F1 chimeras infected with LP-BM5 MuLV developed MAIDS and became completely immune suppressed. These results, coupled with previous studies, indicate resistance or sensitivity to disease is an inherent property of the hematopoietic system that can be transferred by bone marrow grafts.

摘要

用LP - BM5鼠白血病病毒(MuLV)感染某些品系的小鼠,如C57BL/6和C57BL/10 [B10],会迅速导致严重且致命的免疫抑制。B10的H2d同基因品系B10.D2对该疾病具有抗性,但B10×B10.D2 F1小鼠易感,这表明疾病敏感性是显性的。为了确定抗病性是否可以通过过继转移给敏感宿主,用LP - BM5病毒攻击辐射嵌合体(B10.D2→B10×B10.D2 F1和F1→F1)。感染的B10.D2→F1嵌合体未出现免疫功能丧失,而感染LP - BM5 MuLV的F1→F1嵌合体则发展为小鼠获得性免疫缺陷综合征(MAIDS)并完全免疫抑制。这些结果,再加上先前的研究,表明对疾病的抗性或敏感性是造血系统的固有特性,可通过骨髓移植进行转移。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验