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  4. Interleukins 7 and 15 Maintain Human T Cell Proliferative Capacity through STAT5 Signaling

Interleukins 7 and 15 Maintain Human T Cell Proliferative Capacity through STAT5 Signaling

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Author(s)
Drake, Adam
•
Kaur, Mandeep
•
Iliopoulou, Bettina P.
•
Phennicie, Ryan
•
Hanson, Amanda
•
Chen, Jianzhu
•
Phennicie, Ryan T.
•
Iliopoulou, Bettina P.
Date Issued
November 2016
Journal
PLOS ONE
Publisher
Public Library of Science
Citation
Drake, Adam, Mandeep Kaur, Bettina P. Iliopoulou, Ryan Phennicie, Amanda Hanson, and Jianzhu Chen. “Interleukins 7 and 15 Maintain Human T Cell Proliferative Capacity through STAT5 Signaling.” Edited by Jose C. Crispin. PLOS ONE 11, no. 11 (November 17, 2016): e0166280.
Version
Final published version
Abstract
T lymphocytes require signals from self-peptides and cytokines, most notably interleukins 7 and 15 (IL-7, IL-15), for survival. While mouse T cells die rapidly if IL-7 or IL-15 is withdrawn, human T cells can survive prolonged withdrawal of IL-7 and IL-15. Here we show that IL-7 and IL-15 are required to maintain human T cell proliferative capacity through the STAT5 signaling pathway. T cells from humanized mice proliferate better if stimulated in the presence of human IL-7 or IL-15 or if T cells are exposed to human IL-7 or IL-15 in mice. Freshly isolated T cells from human peripheral blood lose proliferative capacity if cultured for 24 hours in the absence of IL-7 or IL-15. We further show that phosphorylation of STAT5 correlates with proliferation and inhibition of STAT5 reduces proliferation. These results reveal a novel role of IL-7 and IL-15 in maintaining human T cell function, provide an explanation for T cell dysfunction in humanized mice, and have significant implications for in vitro studies with human T cells.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution 4.0 International License
http://creativecommons.org/licenses/by/4.0/
Persistent DSpace Link
http://hdl.handle.net/1721.1/107955
DOI of Published Version
http://dx.doi.org/10.1371/journal.pone.0166280
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