Lipid-Reactive T Cells in Immunological Disorders of the Lung
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ryu, Seungwon | - |
dc.contributor.author | Park, Joon Seok | - |
dc.contributor.author | Kim, Hye Young | - |
dc.contributor.author | Kim, Ji Hyung | - |
dc.date.accessioned | 2021-09-02T06:16:51Z | - |
dc.date.available | 2021-09-02T06:16:51Z | - |
dc.date.created | 2021-06-16 | - |
dc.date.issued | 2018-09-26 | - |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/73055 | - |
dc.description.abstract | Regulation of T cell-mediated immunity in the lungs is critical for prevention of immune-related lung disorders and for host protection from pathogens. While the prevalent view of pulmonary T cell responses is based on peptide recognition by antigen receptors, called T cell receptors (TCR), on the T cell surface in the context of classical major histocompatibility complex (MHC) molecules, novel pathways involving the presentation of lipid antigens by cluster of differentiation 1 (CD1) molecules to lipid-reactive T cells are emerging as key players in pulmonary immune system. Whereas, genetic conservation of group II CD1 (CD1d) in mouse and human genomes facilitated numerous in vivo studies of CD1d-restricted invariant natural killer T (i NKT) cells in lung diseases, the recent development of human CD1-transgenic mice has made it possible to examine the physiological roles of group I CD1 (CD1a-c) molecules in lung immunity. Here, we discuss current understanding of the biology of CD1-reactive T cells with a specific focus on their roles in several pulmonary disorders. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.subject | INVARIANT NKT CELLS | - |
dc.subject | CD1 ANTIGEN PRESENTATION | - |
dc.subject | INNATE IMMUNE-RESPONSE | - |
dc.subject | A VIRUS-INFECTION | - |
dc.subject | ALPHA-GALACTOSYLCERAMIDE | - |
dc.subject | DENDRITIC CELLS | - |
dc.subject | AIRWAY INFLAMMATION | - |
dc.subject | PHASE-I | - |
dc.subject | PULMONARY-FIBROSIS | - |
dc.subject | POTENTIAL-ROLE | - |
dc.title | Lipid-Reactive T Cells in Immunological Disorders of the Lung | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Ji Hyung | - |
dc.identifier.doi | 10.3389/fimmu.2018.02205 | - |
dc.identifier.scopusid | 2-s2.0-85054889143 | - |
dc.identifier.wosid | 000445662600002 | - |
dc.identifier.bibliographicCitation | FRONTIERS IN IMMUNOLOGY, v.9 | - |
dc.relation.isPartOf | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.title | FRONTIERS IN IMMUNOLOGY | - |
dc.citation.volume | 9 | - |
dc.type.rims | ART | - |
dc.type.docType | Review | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.subject.keywordPlus | INVARIANT NKT CELLS | - |
dc.subject.keywordPlus | CD1 ANTIGEN PRESENTATION | - |
dc.subject.keywordPlus | INNATE IMMUNE-RESPONSE | - |
dc.subject.keywordPlus | A VIRUS-INFECTION | - |
dc.subject.keywordPlus | ALPHA-GALACTOSYLCERAMIDE | - |
dc.subject.keywordPlus | DENDRITIC CELLS | - |
dc.subject.keywordPlus | AIRWAY INFLAMMATION | - |
dc.subject.keywordPlus | PHASE-I | - |
dc.subject.keywordPlus | PULMONARY-FIBROSIS | - |
dc.subject.keywordPlus | POTENTIAL-ROLE | - |
dc.subject.keywordAuthor | pulmonary disorders | - |
dc.subject.keywordAuthor | lipid antigens | - |
dc.subject.keywordAuthor | CD1 molecules | - |
dc.subject.keywordAuthor | CD1-restricted T cells | - |
dc.subject.keywordAuthor | natural killer T cells | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea 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.