The transcription factor c-Myb regulates CD8+ T cell stemness and antitumor immunity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-03

AUTHORS

Sanjivan Gautam, Jessica Fioravanti, Wei Zhu, John B. Le Gall, Philip Brohawn, Neal E. Lacey, Jinhui Hu, James D. Hocker, Nga Voong Hawk, Veena Kapoor, William G. Telford, Devikala Gurusamy, Zhiya Yu, Avinash Bhandoola, Hai-Hui Xue, Rahul Roychoudhuri, Brandon W. Higgs, Nicholas P. Restifo, Timothy P. Bender, Yun Ji, Luca Gattinoni

ABSTRACT

Stem cells are maintained by transcriptional programs that promote self-renewal and repress differentiation. Here, we found that the transcription factor c-Myb was essential for generating and maintaining stem cells in the CD8+ T cell memory compartment. Following viral infection, CD8+ T cells lacking Myb underwent terminal differentiation and generated fewer stem cell-like central memory cells than did Myb-sufficient T cells. c-Myb acted both as a transcriptional activator of Tcf7 (which encodes the transcription factor Tcf1) to enhance memory development and as a repressor of Zeb2 (which encodes the transcription factor Zeb2) to hinder effector differentiation. Domain-mutagenesis experiments revealed that the transactivation domain of c-Myb was necessary for restraining differentiation, whereas its negative regulatory domain was critical for cell survival. Myb overexpression enhanced CD8+ T cell memory formation, polyfunctionality and recall responses that promoted curative antitumor immunity after adoptive transfer. These findings identify c-Myb as a pivotal regulator of CD8+ T cell stemness and highlight its therapeutic potential. More... »

PAGES

337-349

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41590-018-0311-z

DOI

http://dx.doi.org/10.1038/s41590-018-0311-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112201640

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30778251


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