首页> 美国卫生研究院文献>Inflammatory Bowel Diseases >Alterations in myeloid dendritic cell innate immune responses in the Gαi2-deficient mouse model of colitis

【2h】

Alterations in myeloid dendritic cell innate immune responses in the Gαi2-deficient mouse model of colitis

机译：结肠炎Gαi2缺陷小鼠模型中髓样树突状细胞先天免疫反应的变化

代理获取

本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。

页面导航

摘要
著录项
相似文献
相关主题

摘要

The G protein alpha subunit type-2 (Gαi2)-deficient mouse develops inflammatory bowel disease (IBD) with increased severity in mice on a 129SvEv (129) background compared to the C57BL/6 (B6) background. By breeding these strains to homozygosity for the first time, it became possible to study innate immunity, in this animal model, with more precision than ever before. We learned that dendritic cell distribution and function are significantly different in the two strains of mice.In contrast to Gαi2^-/- B6, Gαi2^-/- 129 mice display accelerated onset and increased severity of colitis, abnormal mucosal DC distribution, accompanied by preponderance for Th1 and Th17-associated gut cytokine expression. TLR9 activation of bone marrow-derived dendritic cells (BMDCs) induces sustained p38 MAPK activation and greater Th1- and Th17-type cytokine secretion in both strains of Gαi2-deficient compared to wild-type BMDCs. However, only B6 Gαi2^-/- BMDCs concomitantly produce IL-10 while Gαi2^-/- 129 BMDCs do not. A relative IL-10 insufficiency in Gαi2^-/- 129 BMDCs may account for the striking difference in disease.

机译：与C57BL / 6（B6）背景相比，G蛋白alpha亚基2型（Gαi2）缺陷小鼠在129SvEv（129）背景下小鼠的炎症性肠病（IBD）严重性增加。通过首次将这些菌株繁殖为纯合子，就有可能在这种动物模型中以前所未有的精度研究先天免疫。我们了解到这两种小鼠的树突状细胞分布和功能存在显着差异。与Gαi2^{-/- B6相比，Gαi2^{-// 129小鼠显示出加速的发作结肠炎的严重程度增加，粘膜DC分布异常，并伴有Th1和Th17相关的肠道细胞因子表达的优势。与野生型BMDC相比，在两种Gαi2缺陷型菌株中，源自骨髓的树突状细胞（BMDC）的TLR9激活均诱导持续的p38 MAPK激活和更大的Th1-和Th17型细胞因子分泌。但是，只有B6Gαi2^{-/- BMDC会同时产生IL-10，而Gαi2^{-/- 129个BMDC则不会。 Gαi2^{-/- 129个BMDC的相对IL-10不足可能是疾病的显着差异。}}}}}

著录项

期刊名称 Inflammatory Bowel Diseases
作者
JA Peña; L Thompson-Snipes; PR Calkins; N Tatevian; M Puppi; MJ Finegold;
展开▼
作者单位

展开▼
年(卷),期 -1(15),2
年度 -1
页码 248–260
总页数 28
原文格式 PDF
正文语种
中图分类肠道病毒与肝炎病毒;肝及胆疾病;肠疾病;
关键词
dendritic cell Gi alpha inflammatory bowel disease cytokine;

机译：树突状细胞;Gi alpha;炎性肠病;细胞因子;

相似文献

外文文献
中文文献
专利

1. Alterations in myeloid dendritic cell innate immune responses in the Galphai2-deficient mouse model of colitis. [J] . Pena JA, Thompson-Snipes L, Calkins PR, Inflammatory bowel diseases . 2009,第2期

机译：骨髓内突细胞的改变在Galphai2缺陷的结肠炎小鼠模型中的粘蛋白树突细胞先天免疫应答。
2. Innate immunity in multiple sclerosis: myeloid dendritic cells in secondary progressive multiple sclerosis are activated and drive a proinflammatory immune response. [J] . Karni A, Abraham M, Monsonego A, The Journal of Immunology: Official Journal of the American Association of Immunologists . 2006,第6期

机译：多发性硬化症的先天免疫：继发性进行性多发性硬化症中的髓样树突状细胞被激活并驱动促炎性免疫反应。
3. Innate Immunity in Multiple Sclerosis: Myeloid Dendritic Cells in Secondary Progressive Multiple Sclerosis Are Activated and Drive a Proinflammatory Immune Response [J] . Arnon Karni, Michal Abraham, Alon Monsonego, The journal of immunology . 2006,第6期

机译：多发性硬化症的先天免疫：继发性进行性多发性硬化症中的髓样树突状细胞被激活并驱动促炎性免疫反应。
4. A mCD3xP-Cadherin Mouse Bispeciflc Allows Immune Profiling of T Cell and Myeloid Cell Populations During Treatment of Syngeneic Mouse Tumor Models [C] . Holly A. Jensen Yongjing Jane Guo, Mary Mileski, Chad Stevens, Protein Engineering Summit. . 2018

机译：MCD3XP-CADHERIN小鼠BISPECIFLC允许在治疗同胞小鼠肿瘤模型期间免疫分析T细胞和骨髓细胞群
5. Checks and Balances: Transcriptional Regulation of Myeloid Innate Immunity and Dendritic Cell Maturation [D] . Nazitto, Rodolfo. 2021

机译：检查和平衡：骨髓内先天免疫和树突细胞成熟的转录调节
6. Correction for Jin et al. BDCA1-Positive Dendritic Cells (DCs) Represent a Unique Human Myeloid DC Subset That Induces Innate and Adaptive Immune Responses to Staphylococcus aureus Infection [O] . Jun-O Jin, Wei Zhang, Jiang-yuan Du, 2015

机译：对Jin等人的校正BDCA1阳性树突状细胞（DCs）代表独特的人类骨髓DC亚集可诱导对金黄色葡萄球菌感染的先天性和适应性免疫反应。
7. Alterations in myeloid dendritic cell innate immune responses in the Gαi2-deficient mouse model of colitis [O] . J. A. Peña, L. Thompson-Snipes, P. R. Calkins, 2009

机译：粘膜炎Gα12缺乏小鼠模型中粘虫树突细胞的改变

Alterations in myeloid dendritic cell innate immune responses in the Gαi2-deficient mouse model of colitis

摘要

著录项

相似文献

相关主题

期刊订阅