IL-2-induced activation-induced cell death is inhibited in IL-15 transgenic mice

被引：362

作者：

Marks-Konczalik, J

Dubois, S

Losi, JM

Sabzevari, H

Yamada, N

Feigenbaum, L

Waldmann, TA

Tagaya, Y ^{[1
]}

机构：

[1] NCI, Frederick Canc Res & Dev Ctr, Metab Branch, Div Clin Sci,NIH, Bethesda, MD 20892 USA

[2] NCI, Frederick Canc Res & Dev Ctr, Tumor Immunol & Biol Lab, Div Basic Sci,NIH, Bethesda, MD 20892 USA

[3] NCI, Frederick Canc Res & Dev Ctr, Dermatol Branch, Div Clin Sci,NIH, Bethesda, MD 20892 USA

[4] NCI, Frederick Canc Res & Dev Ctr, Transgen Mouse Model, Sci Applicat Int Corp Frederick,NIH, Bethesda, MD 20892 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2000年 / 97卷 / 21期

关键词：

D O I：

10.1073/pnas.200363097

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

A transgenic (Tg) mouse expressing human IL-15 was generated to define the role of IL-15 in the normal immune response. Overexpression of IL-15 resulted in an increase of NK, CD44(hi)CD8 memory T cells, and gamma delta T cells. Additionally, we observed the emergence of a novel type of NK-T cells with CD8 alpha alpha' expression. Due to the expansion and activation of NK cells, the IL-15Tg mouse showed enhanced innate immunity. In adaptive T cell immunity, the roles of IL-15 contrasted with those of IL-2. IL-15 inhibited IL-2-induced T cell death, which plays a role in the maintenance of peripheral self-tolerance. IL-15 thus seems to contribute to enhanced immune memory by selectively propagating memory T cells and by blocking T cell death mediated by IL-2.

引用

页码：11445 / 11450

页数：6

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