Item request has been placed!
×
Item request cannot be made.
×
Processing Request
The Notch signaling pathway controls CD8+ T cell differentiation independently of the classical effector HES1.
Item request has been placed!
×
Item request cannot be made.
×
Processing Request
- Additional Information
- Source:
Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
- Publication Information:
Original Publication: San Francisco, CA : Public Library of Science
- Subject Terms:
- Abstract:
During CD8+ T cell response, Notch signaling controls short-lived-effector-cell (SLEC) generation, but the exact mechanisms by which it does so remains unclear. The Notch signaling pathway can act as a key regulator of Akt signaling via direct transcriptional induction of Hes1, which will then repress the transcription of Pten, an inhibitor of Akt signaling. As both Notch and Akt signaling can promote effector CD8+ T cell differentiation, we asked whether Notch signaling influences SLEC differentiation via the HES1-PTEN axis. Here, we demonstrate that HES1 deficiency in murine CD8+ T cells did not impact SLEC differentiation. Moreover, we show that Pten transcriptional repression in effector CD8+ T cells is not mediated by Notch signaling although Akt activation requires Notch signaling. Therefore, HES1 is not an effector of Notch signaling during CD8+ T cell response.
Competing Interests: The authors have declared that no competing interests exist.
- References:
J Clin Invest. 2017 Apr 3;127(4):1574-1588. (PMID: 28319044)
J Immunol. 2012 May 1;188(9):4305-14. (PMID: 22467649)
Cell Death Differ. 2009 Jun;16(6):879-89. (PMID: 19265851)
J Immunol. 2015 Jun 15;194(12):5654-62. (PMID: 25972473)
Nat Immunol. 2005 Sep;6(9):881-8. (PMID: 16056227)
Nat Immunol. 2008 Oct;9(10):1091-4. (PMID: 18800157)
Nat Immunol. 2015 Nov;16(11):1162-73. (PMID: 26437242)
Nat Immunol. 2008 Oct;9(10):1140-7. (PMID: 18724371)
Cell. 1994 Jan 14;76(1):17-27. (PMID: 8287475)
Nature. 2009 Jul 2;460(7251):108-12. (PMID: 19543266)
Blood. 2012 Aug 16;120(7):1439-48. (PMID: 22649105)
J Immunol. 2014 Aug 15;193(4):1847-54. (PMID: 25015830)
Immunity. 2010 Nov 24;33(5):671-84. (PMID: 21093323)
Development. 2008 Aug;135(15):2531-41. (PMID: 18579678)
Nat Rev Immunol. 2012 Nov;12(11):749-61. (PMID: 23080391)
Immunity. 2011 Feb 25;34(2):224-36. (PMID: 21295499)
PLoS One. 2012;7(1):e30139. (PMID: 22291907)
J Immunol. 2005 Oct 1;175(7):4400-7. (PMID: 16177081)
Blood. 2007 Jul 1;110(1):278-86. (PMID: 17363738)
J Leukoc Biol. 2007 Sep;82(3):645-56. (PMID: 17554014)
Immunity. 2010 Jan 29;32(1):67-78. (PMID: 20060330)
Infect Immun. 2006 Nov;74(11):6387-97. (PMID: 16954391)
Cell Rep. 2016 Feb 9;14(5):1206-1217. (PMID: 26804903)
Nat Immunol. 2014 Dec;15(12):1143-51. (PMID: 25344724)
- Grant Information:
PJT-14903 Canada CIHR; PJT-152988 Canada CIHR
- Accession Number:
0 (Hes1 protein, mouse)
0 (Receptors, Notch)
0 (Transcription Factor HES-1)
EC 3.1.3.67 (PTEN Phosphohydrolase)
EC 3.1.3.67 (Pten protein, mouse)
- Publication Date:
Date Created: 20190406 Date Completed: 20191223 Latest Revision: 20200309
- Publication Date:
20231215
- Accession Number:
PMC6450647
- Accession Number:
10.1371/journal.pone.0215012
- Accession Number:
30951556
No Comments.