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

被引：49

作者：

Minagawa, M

Watanabe, H

Miyaji, C

Tomiyama, K

Shimura, H

Ito, A

Ito, M

Domen, J

Weissman, IL

Kawai, K

机构：

[1] Niigata Univ, Sch Med, Dept Dermatol, Niigata 9518510, Japan

[2] Niigata Univ, Sch Med, Dept Immunol, Niigata 9518510, Japan

[3] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA

[4] Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA

来源：

JOURNAL OF IMMUNOLOGY | 2002年 / 169卷 / 08期

关键词：

D O I：

10.4049/jimmunol.169.8.4153

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：4153 / 4160

页数：8

共 101 条

[1] Transduction of interleukin-2 antiapoptotic and proliferative signals via Akt protein kinase [J].