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Enforced Expression of Bcl-2 Restores the Number of NK Cells, But Does Not Rescue the Impaired Development of NKT Cells or Intraepithelial Lymphocytes, in IL-2/IL-15 Receptor β-Chain-Deficient Mice
Author(s) -
Masahiro Minagawa,
Hisami Watanabe,
Chikako Miyaji,
Katsuhiro Tomiyama,
Hideki Shimura,
Akiko Ito,
Masaaki Ito,
Jos Domen,
Irving L. Weissman,
Kazuhiro Kawai
Publication year - 2002
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.169.8.4153
Subject(s) - intraepithelial lymphocyte , interleukin 15 , biology , immunology , cytotoxic t cell , natural killer t cell , interleukin 12 , transgene , genetically modified mouse , innate lymphoid cell , lymphocyte , interleukin 21 , cancer research , microbiology and biotechnology , innate immune system , interleukin , t cell , immune system , cytokine , gene , in vitro , biochemistry
IL-2/IL-15Rbeta-deficient mice display impaired development of NK cells, NKT cells, and intraepithelial lymphocytes of the intestine and skin. To determine the role of survival signals mediated by IL-2/IL-15R in the development of these innate lymphocytes, we introduced a bcl-2 transgene into IL-2/IL-15Rbeta-deficient mice. Enforced expression of Bcl-2 restored the number of NK cells in IL-2/IL-15Rbeta-deficient mice, but the rescued NK cells showed no cytotoxic activity. The numbers of NKT cells and intestinal intraepithelial lymphocytes did not increase significantly, and skin intraepithelial lymphocytes remained undetectable in the bcl-2 transgenic IL-2/IL-15Rbeta-deficient mice. These results indicate an essential role of IL-2/IL-15R-mediated survival signals in the development of NK cells, but they also show that additional nonsurvival signals from IL-2/IL-15R are necessary for innate lymphocyte development.

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