• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

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

造血细胞足以引发 POLB-Y265C 突变导致的狼疮。

The hematopoietic compartment is sufficient for lupus development resulting from the POLB-Y265C mutation.

机构信息

Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT, United States of America.

Department of Cellular and Molecular Medicine and University of Arizona Cancer Center, Tucson, AZ, United States of America.

出版信息

PLoS One. 2022 Apr 29;17(4):e0267913. doi: 10.1371/journal.pone.0267913. eCollection 2022.

DOI:10.1371/journal.pone.0267913
PMID:35486639
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9053796/
Abstract

Systemic lupus erythematosus is a chronic disease characterized by autoantibodies, renal and cutaneous disease, and immune complex formation. Emerging evidence suggests that aberrant DNA repair is an underlying mechanism of lupus development. We previously showed that the POLBY265C/C mutation, which results in development of an aberrant immune repertoire, leads to lupus-like disease in mice. To address whether the hematopoietic compartment is sufficient for lupus development, we transplanted bone marrow cells from POLBY265C/C and POLB+/+ into wild-type congenic mice. Only mice transplanted with the POLBY265C/C bone marrow develop high levels of antinuclear antibodies and renal disease. In conclusion, we show that the hematopoietic compartment harvested from the POLBY265C/C mice is sufficient for development of autoimmune disease.

摘要

系统性红斑狼疮是一种以自身抗体、肾脏和皮肤疾病以及免疫复合物形成为特征的慢性疾病。新出现的证据表明,异常的 DNA 修复是狼疮发展的潜在机制。我们之前曾表明,POLBY265C/C 突变导致异常免疫受体的产生,导致小鼠发生狼疮样疾病。为了确定造血细胞是否足以引起狼疮的发生,我们将 POLBY265C/C 和 POLB+/+的骨髓细胞移植到野生型同基因小鼠中。只有接受 POLBY265C/C 骨髓移植的小鼠才会产生高水平的抗核抗体和肾脏疾病。总之,我们表明,从 POLBY265C/C 小鼠中采集的造血细胞足以发展自身免疫性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/b019b6f47842/pone.0267913.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/b9e75e6c0964/pone.0267913.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/c78a58025d43/pone.0267913.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/b019b6f47842/pone.0267913.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/b9e75e6c0964/pone.0267913.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/c78a58025d43/pone.0267913.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a8a0/9053796/b019b6f47842/pone.0267913.g003.jpg

相似文献

1
The hematopoietic compartment is sufficient for lupus development resulting from the POLB-Y265C mutation.造血细胞足以引发 POLB-Y265C 突变导致的狼疮。
PLoS One. 2022 Apr 29;17(4):e0267913. doi: 10.1371/journal.pone.0267913. eCollection 2022.
2
DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model.在Polb - Y265C小鼠模型中,DNA糖基化酶缺乏导致狼疮严重程度降低。
DNA Repair (Amst). 2021 Sep;105:103152. doi: 10.1016/j.dnarep.2021.103152. Epub 2021 Jun 24.
3
Mutation of POLB causes lupus in mice.POLB 突变导致小鼠狼疮。
Cell Rep. 2014 Jan 16;6(1):1-8. doi: 10.1016/j.celrep.2013.12.017. Epub 2014 Jan 2.
4
Linkage analysis of systemic lupus erythematosus induced in diabetes-prone nonobese diabetic mice by Mycobacterium bovis.牛分枝杆菌诱导的糖尿病易感性非肥胖糖尿病小鼠系统性红斑狼疮的连锁分析。
J Immunol. 2000 Aug 1;165(3):1673-84. doi: 10.4049/jimmunol.165.3.1673.
5
Toll-like receptor 8 deletion accelerates autoimmunity in a mouse model of lupus through a Toll-like receptor 7-dependent mechanism.Toll样受体8缺失通过Toll样受体7依赖性机制加速狼疮小鼠模型中的自身免疫反应。
Immunology. 2015 May;145(1):60-70. doi: 10.1111/imm.12426.
6
Autoantibodies and their idiotypes.自身抗体及其独特型。
Curr Opin Rheumatol. 1992 Oct;4(5):635-43.
7
Impaired B cell anergy is not sufficient to breach tolerance to nuclear antigen in Vκ8/3H9 lupus-prone mice.B 细胞失能不足以打破 Vκ8/3H9 狼疮易感小鼠对核抗原的耐受。
PLoS One. 2020 Jul 28;15(7):e0236664. doi: 10.1371/journal.pone.0236664. eCollection 2020.
8
Molecular, metabolic and immune evidence suggest that systemic autoimmune disease is antigen-mediated.分子、代谢及免疫方面的证据表明,系统性自身免疫性疾病是由抗原介导的。
Med Hypotheses. 1996 Nov;47(5):337-46. doi: 10.1016/s0306-9877(96)90214-5.
9
Evidence for genes in addition to Tlr7 in the Yaa translocation linked with acceleration of systemic lupus erythematosus.除Tlr7外,Yaa易位中与系统性红斑狼疮加速相关的基因的证据。
J Immunol. 2008 Jul 15;181(2):1556-62. doi: 10.4049/jimmunol.181.2.1556.
10
Strain-Specific Manifestation of Lupus-like Systemic Autoimmunity Caused by Mutation.突变导致的狼疮样系统性自身免疫的菌株特异性表现。
J Immunol. 2019 Jun 1;202(11):3161-3172. doi: 10.4049/jimmunol.1801159. Epub 2019 Apr 24.

引用本文的文献

1
Mouse models to explore the biological and organismic role of DNA polymerase beta.探索 DNA 聚合酶β的生物学和机体作用的小鼠模型。
Environ Mol Mutagen. 2024 Apr;65 Suppl 1(Suppl 1):57-71. doi: 10.1002/em.22593.

本文引用的文献

1
DNA polymerase beta participates in DNA End-joining.DNA 聚合酶β参与 DNA 末端连接。
Nucleic Acids Res. 2018 Jan 9;46(1):242-255. doi: 10.1093/nar/gkx1147.
2
DNA polymerase β: A missing link of the base excision repair machinery in mammalian mitochondria.DNA聚合酶β:哺乳动物线粒体碱基切除修复机制中缺失的一环。
DNA Repair (Amst). 2017 Dec;60:77-88. doi: 10.1016/j.dnarep.2017.10.011. Epub 2017 Oct 28.
3
DNA repair and systemic lupus erythematosus.DNA修复与系统性红斑狼疮
DNA Repair (Amst). 2017 Aug;56:174-182. doi: 10.1016/j.dnarep.2017.06.020. Epub 2017 Jun 9.
4
DNA Polymerase Beta Participates in Mitochondrial DNA Repair.DNA聚合酶β参与线粒体DNA修复。
Mol Cell Biol. 2017 Jul 28;37(16). doi: 10.1128/MCB.00237-17. Print 2017 Aug 15.
5
Oxidation events and skin aging.氧化事件与皮肤衰老。
Ageing Res Rev. 2015 May;21:16-29. doi: 10.1016/j.arr.2015.01.001. Epub 2015 Jan 31.
6
Mutation of POLB causes lupus in mice.POLB 突变导致小鼠狼疮。
Cell Rep. 2014 Jan 16;6(1):1-8. doi: 10.1016/j.celrep.2013.12.017. Epub 2014 Jan 2.
7
Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus.系统性红斑狼疮国际协作临床分类标准的推导与验证
Arthritis Rheum. 2012 Aug;64(8):2677-86. doi: 10.1002/art.34473.
8
Y265C DNA polymerase beta knockin mice survive past birth and accumulate base excision repair intermediate substrates.Y265C DNA 聚合酶β基因敲入小鼠可存活至出生后,并积累碱基切除修复中间产物。
Proc Natl Acad Sci U S A. 2012 Apr 24;109(17):6632-7. doi: 10.1073/pnas.1200800109. Epub 2012 Apr 9.
9
Base excision repair and cancer.碱基切除修复与癌症。
Cancer Lett. 2012 Dec 31;327(1-2):73-89. doi: 10.1016/j.canlet.2011.12.038. Epub 2012 Jan 15.
10
Follow-up study identifies two novel susceptibility loci PRKCB and 8p11.21 for systemic lupus erythematosus.后续研究确定了两个新的系统性红斑狼疮易感性基因座 PRKCB 和 8p11.21。
Rheumatology (Oxford). 2011 Apr;50(4):682-8. doi: 10.1093/rheumatology/keq313. Epub 2010 Dec 6.