Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation
文献类型：期刊论文
| 作者 | Li, Jingyu2; Shi, Wenli2; Ji, Yan2; Cai, Ting2; Qiu, Ju2; Sung, Hanxiao1; Chen, Yuqin1; Sheng, Huiming1; Shu, Jie1; Guo, Xiaohuan4,5,6 |
| 刊名 | NATURE COMMUNICATIONS
 |
| 出版日期 | 2019 |
| 卷号 | 10期号:-页码:3371 |
| ISSN号 | 2041-1723 |
| 关键词 | cancer-associated cachexia adipose tissue loss long noncoding RNAs adipogenesis HuR |
| DOI | 10.1038/s41467-019-11304-8 |
| 文献子类 | Article |
| 英文摘要 | TNF-like ligand 1 A (TL1A) and death receptor 3 (DR3) are a ligand-receptor pair involved in the pathogenesis of inflammatory bowel disease. Group 3 innate lymphoid cells (ILC3s) regulate intestinal immunity and highly express DR3. Here, we report that activation of DR3 signaling by an agonistic anti-DR3 antibody increases GM-CSF production from ILC3s through the p38 MAPK pathway. GM-CSF causes accumulation of eosinophils, neutrophils and CD11b(+)CD11c(+) myeloid cells, resulting in loss of ILC3s from the intestine in an IL-23-dependent manner and exacerbating colitis. Blockade of GM-CSF or IL-23 reverses anti-DR3 antibody-driven ILC3 loss, whereas overexpression of IL-23 induces loss of ILC3s in the absence of GM-CSF. Neutralization of TL1A by soluble DR3 ameliorates both DSS and anti-CD40 antibody-induced colitis. Moreover, ILC3s are required for the deleterious effect of anti-DR3 antibodies on innate colitis. These findings clarify the process and consequences of DR3 signaling-induced intestinal inflammation through regulation of ILC3s. |
| 学科主题 | Science & Technology - Other Topics |
| WOS关键词 | INNATE LYMPHOID-CELLS ; TNF-LIKE LIGAND ; ROR-GAMMA-T ; CYTOKINE TL1A ; MUCOSAL ; EXPRESSION ; COLITIS ; IL-23 ; SUSCEPTIBILITY ; EXPANSION |
| 语种 | 英语 |
| 出版者 | NATURE PUBLISHING GROUP |
| WOS记录号 | WOS:000477706000010 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/544]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Shanghai Jiao Tong Univ, Tongren Hosp, Sch Med, Shanghai 200336, Peoples R China; 2.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Nutr & Hlth, Shanghai Inst Biol Sci,CAS Key Lab Tissue Microen, Shanghai 200031, Peoples R China; 3.Univ Florida, Coll Vet Med, Dept Infect Dis & Immunol, Gainesville, FL 32608 USA, 4.Tsinghua Univ, Beijing Key Lab Immunol Res Chron Dis, Beijing 100084, Peoples R China; 5.Tsinghua Univ, Sch Med, Dept Basic Med Sci, Beijing 100084, Peoples R China; 6.Tsinghua Univ, Inst Immunol, Beijing 100084, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Li, Jingyu,Shi, Wenli,Ji, Yan,et al. Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation[J]. NATURE COMMUNICATIONS,2019,10(-):3371. |
| APA | Li, Jingyu.,Shi, Wenli.,Ji, Yan.,Cai, Ting.,Qiu, Ju.,...&,.(2019).Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation.NATURE COMMUNICATIONS,10(-),3371. |
| MLA | Li, Jingyu,et al."Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation".NATURE COMMUNICATIONS 10.-(2019):3371. |
入库方式： OAI收割
来源：上海营养与健康研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。