The protective roles of integrin α4β7 and Amphiregulin-expressing innate lymphoid cells in lupus nephritis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ryu, Seungwon | - |
dc.contributor.author | Kim, Kyung Ah | - |
dc.contributor.author | Kim, Jinwoo | - |
dc.contributor.author | Lee, Dong Hun | - |
dc.contributor.author | Bae, Yong-Soo | - |
dc.contributor.author | Lee, Hajeong | - |
dc.contributor.author | Kim, Byoung Choul | - |
dc.contributor.author | Kim, Hye Young | - |
dc.date.accessioned | 2024-07-21T12:30:23Z | - |
dc.date.available | 2024-07-21T12:30:23Z | - |
dc.date.issued | 2024-07 | - |
dc.identifier.issn | 1672-7681 | - |
dc.identifier.issn | 2042-0226 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/92043 | - |
dc.description.abstract | Type 2 innate lymphoid cells (ILC2s) have emerged as key regulators of the immune response in renal inflammatory diseases such as lupus nephritis. However, the mechanisms underlying ILC2 adhesion and migration in the kidney remain poorly understood. Here, we revealed the critical role of integrin alpha 4 beta 7 in mediating renal ILC2 adhesion and function. We found that integrin alpha 4 beta 7 enables the retention of ILC2s in the kidney by binding to VCAM-1, E-cadherin, or fibronectin on structural cells. Moreover, integrin alpha 4 beta 7 knockdown reduced the production of the reparative cytokine amphiregulin (Areg) by ILC2s. In lupus nephritis, TLR7/9 signaling within the kidney microenvironment downregulates integrin alpha 4 beta 7 expression, leading to decreased Areg production and promoting the egress of ILC2s. Notably, IL-33 treatment upregulated integrin alpha 4 beta 7 and Areg expression in ILC2s, thereby enhancing survival and reducing inflammation in lupus nephritis. Together, these findings highlight the potential of targeting ILC2 adhesion as a therapeutic strategy for autoimmune kidney diseases. | - |
dc.format.extent | 15 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | CHIN SOCIETY IMMUNOLOGY | - |
dc.title | The protective roles of integrin α4β7 and Amphiregulin-expressing innate lymphoid cells in lupus nephritis | - |
dc.type | Article | - |
dc.identifier.wosid | 001234274600001 | - |
dc.identifier.doi | 10.1038/s41423-024-01178-2 | - |
dc.identifier.bibliographicCitation | CELLULAR & MOLECULAR IMMUNOLOGY, v.21, no.7, pp 723 - 737 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.scopusid | 2-s2.0-85194566256 | - |
dc.citation.endPage | 737 | - |
dc.citation.startPage | 723 | - |
dc.citation.title | CELLULAR & MOLECULAR IMMUNOLOGY | - |
dc.citation.volume | 21 | - |
dc.citation.number | 7 | - |
dc.type.docType | Article | - |
dc.publisher.location | 중국 | - |
dc.subject.keywordAuthor | Innate lymphoid cells | - |
dc.subject.keywordAuthor | Tissue residency | - |
dc.subject.keywordAuthor | Adhesion molecules | - |
dc.subject.keywordAuthor | Integrins | - |
dc.subject.keywordAuthor | Kidney | - |
dc.subject.keywordAuthor | Lupus nephritis | - |
dc.subject.keywordAuthor | Amphiregulin | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordPlus | IMMUNITY | - |
dc.subject.keywordPlus | IL-33 | - |
dc.subject.keywordPlus | AUTOIMMUNITY | - |
dc.subject.keywordPlus | TRAFFICKING | - |
dc.subject.keywordPlus | HOMEOSTASIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPANSION | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
1342, Seongnam-daero, Sujeong-gu, Seongnam-si, Gyeonggi-do, Republic of Korea(13120)031-750-5114
COPYRIGHT 2020 Gachon University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.