https://scholars.lib.ntu.edu.tw/handle/123456789/414593
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Chi, Hsi-Hua | en_US |
dc.contributor.author | Hua, Kuo-Feng | en_US |
dc.contributor.author | Lin, Yu-Chuan | en_US |
dc.contributor.author | CHING-LIANG CHU | en_US |
dc.contributor.author | Hsieh, Chih-Yu | en_US |
dc.contributor.author | Hsu, Yu-Juei | en_US |
dc.contributor.author | Ka, Shuk-Man | en_US |
dc.contributor.author | Tsai, Yu-Ling | en_US |
dc.contributor.author | Liu, Feng-Cheng | en_US |
dc.contributor.author | Chen, Ann | en_US |
dc.creator | Chi, Hsi-Hua;Hua, Kuo-Feng;Lin, Yu-Chuan;Ching-Liang Chu;Hsieh, Chih-Yu;Hsu, Yu-Juei;Ka, Shuk-Man;Tsai, Yu-Ling;Liu, Feng-Cheng;Chen, Ann | - |
dc.date.accessioned | 2019-07-23T07:33:58Z | - |
dc.date.available | 2019-07-23T07:33:58Z | - |
dc.date.issued | 2017-07 | - |
dc.identifier.issn | 1046-6673 | - |
dc.identifier.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-85021712319&partnerID=MN8TOARS | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/414593 | - |
dc.description.abstract | IL-36 cytokines are proinflammatory and have an important role in innate and adaptive immunity, but the role of IL-36 signaling in renal tubulointerstitial lesions (TILs), a major prognostic feature of renal inflammation and fibrosis, remains undetermined. In this study, increased IL-36α expression detected in renal biopsy specimens and urine samples from patients with renal TILs correlated with renal function impairment. We confirmed the increased expression of IL-36α in the renal tubular epithelial cells of a mouse model of unilateral ureteral obstruction (UUO) and related cell models using mechanically induced pressure, oxidative stress, or high mobility group box 1. In contrast, the kidneys of IL-36 receptor (IL-36R) knockout mice exhibit attenuated TILs after UUO. Compared with UUO-treated wild-type mice, UUO-treated IL-36 knockout mice exhibited markedly reduced NLRP3 inflammasome activation and macrophage/T cell infiltration in the kidney and T cell activation in the renal draining lymph nodes. In vitro, recombinant IL-36α facilitated NLRP3 inflammasome activation in renal tubular epithelial cells, macrophages, and dendritic cells and enhanced dendritic cell-induced T cell proliferation and Th17 differentiation. Furthermore, deficiency of IL-23, which was diminished in IL-36R knockout UUO mice, also reduced renal TIL formation in UUO mice. In wild-type mice, administration of an IL-36R antagonist after UUO reproduced the results obtained in UUO-treated IL-36R knockout mice. We propose that IL-36 signaling contributes to the pathogenesis of renal TILs through the activation of the NLRP3 inflammasome and IL-23/IL-17 axis. | en_US |
dc.language.iso | en | en_US |
dc.publisher | AMER SOC NEPHROLOGY | en_US |
dc.relation.ispartof | Journal of the American Society of Nephrology : JASN | en_US |
dc.subject | IL-36 receptor; IL-36 receptor antagonist; IL-36α; knockout mice; patients’ samples; unilateral ureteral obstruction | en_US |
dc.title | IL-36 Signaling Facilitates Activation of the NLRP3 Inflammasome and IL-23/IL-17 Axis in Renal Inflammation and Fibrosis | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1681/ASN.2016080840 | - |
dc.identifier.pmid | 28179433 | - |
dc.identifier.scopus | 2-s2.0-85021712319 | - |
dc.identifier.isi | WOS:000404568700011 | - |
dc.identifier.url | https://api.elsevier.com/content/abstract/scopus_id/85021712319 | - |
dc.relation.pages | 2022 | en_US |
dc.relation.journalvolume | 28 | en_US |
dc.relation.journalissue | 7 | en_US |
dc.relation.pageend | 2037 | en_US |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.languageiso639-1 | en | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
crisitem.author.dept | Immunology | - |
crisitem.author.orcid | 0000-0002-8463-526X | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 免疫學研究所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。