期刊
SCIENCE
卷 335, 期 6071, 页码 984-989出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1215418
关键词
-
资金
- Bundesministerium fur Bildung und Forschung (BMBF)-FORSYS
- National Health and Medical Research Council
- German Research Foundation [GRK1121, SFB618, SFB650]
- Science Foundation Ireland
- Program for Improvement of Research Environment for Young Researchers
- Japanese Ministry of Education, Culture, Sports, Science and Technology
- Japan Science and Technology Agency, PRESTO
- BMBF (NGFNplus) [FKZ PIM-01GS0802-3]
- Wilhelm Sander-Stiftung
- Volkswagen Foundation
- Fondation Leenaards
- European Community
- Swiss National Science Foundation
- Grants-in-Aid for Scientific Research [21390303, 23390262] Funding Source: KAKEN
Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as damage-associated molecular patterns or alarmins, remains ill defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8(+) T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a CTL-intrinsic fashion, determined plurifunctional effector cell differentiation, and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据