Open AccessReprogramming of T Cells to Natural Killer–Like Cells upon Bcl11b Deletion
Author(s) -
Peng Li,
Shan Burke,
Juexuan Wang,
Xiongfeng Chen,
Mariaestela Ortiz,
Song-Choon Lee,
Dong Lu,
Lia S. Campos,
David Goulding,
Bee Ling Ng,
Gordon Dougan,
Brian J.P. Huntly,
Berthold Göttgens,
Nancy A. Jenkins,
Neal G. Copeland,
Francesco Colucci,
Pentao Liu
Publication year - 2010
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.1188063
Subject(s) - biology , reprogramming , acquired immune system , microbiology and biotechnology , immune system , interleukin 21 , lymphokine activated killer cell , innate lymphoid cell , natural killer cell , natural killer t cell , interleukin 12 , innate immune system , t cell , cytotoxic t cell , cell , immunology , in vitro , genetics
T cells develop in the thymus and are critical for adaptive immunity. Natural killer (NK) lymphocytes constitute an essential component of the innate immune system in tumor surveillance, reproduction, and defense against microbes and viruses. Here, we show that the transcription factor Bcl11b was expressed in all T cell compartments and was indispensable for T lineage development. When Bcl11b was deleted, T cells from all developmental stages acquired NK cell properties and concomitantly lost or decreased T cell-associated gene expression. These induced T-to-natural killer (ITNK) cells, which were morphologically and genetically similar to conventional NK cells, killed tumor cells in vitro, and effectively prevented tumor metastasis in vivo. Therefore, ITNKs may represent a new cell source for cell-based therapies.
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