Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 양철수 | - |
dc.date.accessioned | 2021-08-31T06:59:50Z | - |
dc.date.available | 2021-08-31T06:59:50Z | - |
dc.date.issued | 2020-08 | - |
dc.identifier.citation | FRONTIERS IN IMMUNOLOGY, v. 11, Article no. 1790, 11pp | en_US |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://www.frontiersin.org/articles/10.3389/fimmu.2020.01790/full | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/164723 | - |
dc.description.abstract | Mycobacterium tuberculosis (Mtb)has complex and intricate interactions with host immune cells.Mtbcan survive, persist, and grow within macrophages and thereby circumvent detection by the innate immune system. Recently, the field of immunometabolism, which focuses on the link between metabolism and immune function, has provided us with an improved understanding of the role of metabolism in modulating immune function. For example, host immune cells can switch from oxidative phosphorylation to glycolysis in response to infection, a phenomenon known as the Warburg effect. In this state, immune cells are capable of amplifying production of both antimicrobial pro-inflammatory mediators that are critical for the elimination of bacteria. Also, cells undergoing the Warburg effect upregulate production of nitric oxide augment the synthesis of bioactive lipids. In this review, we describe our current understanding of the Warburg effect and discuss its role in promoting host immune responses toMtb. In most settings, immune cells utilize the Warburg effect to promote inflammation and thereby eliminate invading bacteria interestingly,Mtbexploits this effect to promote its own survival. A better understanding of the dynamics of metabolism within immune cells together with the specific features that contribute to the pathogenesis of tuberculosis (TB) may suggest potential host-directed therapeutic targets for promoting clearance ofMtband limiting its survivalin vivo. | en_US |
dc.description.sponsorship | This work was supported by the NRF grant funded by the Korea government (MSIP) (2016R1D1A1A02937312 and 2019R1I1A2A01064237); a grant from the KHIDI, funded by the Ministry of Health & Welfare, Republic of Korea (HI16C1653). We would like to thank all members of the Infection Biology Lab for critical reading and discussion of the manuscript. | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | FRONTIERS MEDIA SA | en_US |
dc.subject | Mycobacterium tuberculosis | en_US |
dc.subject | innate immunity | en_US |
dc.subject | immunometabolism | en_US |
dc.subject | host-directed therapy | en_US |
dc.subject | inflammation | en_US |
dc.title | Host-Directed Therapy in Tuberculosis: Targeting Host Metabolism | en_US |
dc.type | Article | en_US |
dc.relation.volume | 11 | - |
dc.identifier.doi | 10.3389/fimmu.2020.01790 | - |
dc.relation.page | 1-11 | - |
dc.relation.journal | FRONTIERS IN IMMUNOLOGY | - |
dc.contributor.googleauthor | Kim, Jae-Sung | - |
dc.contributor.googleauthor | Kim, Ye-Ram | - |
dc.contributor.googleauthor | Yang, Chul-Su | - |
dc.relation.code | 2020050760 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF SCIENCE AND CONVERGENCE TECHNOLOGY[E] | - |
dc.sector.department | DEPARTMENT OF MOLECULAR AND LIFE SCIENCE | - |
dc.identifier.pid | chulsuyang | - |
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