T cell stemness and dysfunction in tumors are triggered by a common mechanism
DC Field | Value | Language |
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dc.contributor.author | Vodnala, Suman Kumar | - |
dc.contributor.author | Eil, Robert | - |
dc.contributor.author | Kishton, Rigel J. | - |
dc.contributor.author | Sukumar, Madhusudhanan | - |
dc.contributor.author | Yamamoto, Tori N. | - |
dc.contributor.author | Ngoc-Han Ha | - |
dc.contributor.author | Lee, Ping-Hsien | - |
dc.contributor.author | Shin, MinHwa | - |
dc.contributor.author | Patel, Shashank J. | - |
dc.contributor.author | Yu, Zhiya | - |
dc.contributor.author | Palmer, Douglas C. | - |
dc.contributor.author | Kruhlak, Michael J. | - |
dc.contributor.author | Liu, Xiaojing | - |
dc.contributor.author | Locasale, Jason W. | - |
dc.contributor.author | Huang, Jing | - |
dc.contributor.author | Roychoudhuri, Rahul | - |
dc.contributor.author | Finkel, Toren | - |
dc.contributor.author | Klebanoff, Christopher A. | - |
dc.contributor.author | Restifo, Nicholas P. | - |
dc.date.accessioned | 2021-09-01T17:11:22Z | - |
dc.date.available | 2021-09-01T17:11:22Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2019-03-29 | - |
dc.identifier.issn | 0036-8075 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/66592 | - |
dc.description.abstract | A paradox of tumor immunology is that tumor-infiltrating lymphocytes are dysfunctional in situ, yet are capable of stem cell-like behavior including self-renewal, expansion, and multipotency, resulting in the eradication of large metastatic tumors. We find that the overabundance of potassium in the tumor microenvironment underlies this dichotomy, triggering suppression of T cell effector function while preserving stemness. High levels of extracellular potassium constrain T cell effector programs by limiting nutrient uptake, thereby inducing autophagy and reduction of histone acetylation at effector and exhaustion loci, which in turn produces CD8(+) T cells with improved in vivo persistence, multipotency, and tumor clearance. This mechanistic knowledge advances our understanding of T cell dysfunction and may lead to novel approaches that enable the development of enhanced T cell strategies for cancer immunotherapy. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER ASSOC ADVANCEMENT SCIENCE | - |
dc.subject | LINEAGE RELATIONSHIP | - |
dc.subject | EXPRESSION ANALYSIS | - |
dc.subject | ACETYL-COENZYME | - |
dc.subject | EFFECTOR | - |
dc.subject | DIFFERENTIATION | - |
dc.subject | IMMUNOTHERAPY | - |
dc.subject | CANCER | - |
dc.subject | MODULATION | - |
dc.subject | SURVIVAL | - |
dc.subject | NECROSIS | - |
dc.title | T cell stemness and dysfunction in tumors are triggered by a common mechanism | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, MinHwa | - |
dc.identifier.doi | 10.1126/science.aau0135 | - |
dc.identifier.scopusid | 2-s2.0-85064134700 | - |
dc.identifier.wosid | 000462738000028 | - |
dc.identifier.bibliographicCitation | SCIENCE, v.363, no.6434, pp.1417 - + | - |
dc.relation.isPartOf | SCIENCE | - |
dc.citation.title | SCIENCE | - |
dc.citation.volume | 363 | - |
dc.citation.number | 6434 | - |
dc.citation.startPage | 1417 | - |
dc.citation.endPage | + | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | LINEAGE RELATIONSHIP | - |
dc.subject.keywordPlus | EXPRESSION ANALYSIS | - |
dc.subject.keywordPlus | ACETYL-COENZYME | - |
dc.subject.keywordPlus | EFFECTOR | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | IMMUNOTHERAPY | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | MODULATION | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | NECROSIS | - |
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