期刊
CELL
卷 144, 期 4, 页码 601-613出版社
CELL PRESS
DOI: 10.1016/j.cell.2011.01.011
关键词
-
资金
- Canadian Institute for Health Research [CIHR-MOP-106529]
- Terry Fox Cancer Foundation National Cancer Institute of Canada
- Boninchi Foundation (Geneva, Switzerland)
- National Cancer Institute of Canada
- Irvington Institute with the Cancer Research Institute (New York, NY)
- Australian National Health and Medical Research Council
- Natural Sciences and Engineering Research Council of Canada
- Ontario Ministry of Health and Long Term Care (OMOHLTC)
Understanding the factors that impede immune responses to persistent viruses is essential in designing therapies for HIV infection. Mice infected with LCMV clone-13 have persistent high-level viremia and a dysfunctional immune response. Interleukin-7, a cytokine that is critical for immune development and homeostasis, was used here to promote immunity toward clone-13, enabling elucidation of the inhibitory pathways underlying impaired antiviral immune response. Mechanistically, IL-7 down-regulated a critical repressor of cytokine signaling, Socs3, resulting in amplified cytokine production, increased T cell effector function and numbers, and viral clearance. IL-7 enhanced thymic output to expand the naive T cell pool, including T cells that were not LCMV specific. Additionally, IL-7 promoted production of cytoprotective IL-22 that abrogated liver pathology. The IL-7-mediated effects were dependent on endogenous IL-6. These attributes of IL-7 have profound implications for its use as a therapeutic in the treatment of chronic viral diseases.
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