期刊
IMMUNOLOGY
卷 119, 期 3, 页码 355-361出版社
WILEY
DOI: 10.1111/j.1365-2567.2006.02439.x
关键词
cellular activation; natural killer cells; natural killer T cells; parasite; protozoan; T lymphocytes
类别
资金
- NIAID NIH HHS [R01 AI049455, AI49455] Funding Source: Medline
The protective immune response against Trypanosoma cruzi is improved by treatment with the natural killer (NK) T-cell glycolipid antigen alpha-galactosylceramide (alpha-GalCer). A single alpha-GalCer treatment of mice before T. cruzi infection decreases parasitaemia and prolongs survival. This protection is dependent on CD1d-restricted NKT cells and interferon-gamma (IFN-gamma) suggesting that alpha-GalCer-activated NKT cells produce IFN-gamma, which stimulates the cells of the innate and adaptive immune responses to provide protection. To learn which cells provide protection we investigate here alpha-GalCer treatment of mice deficient in different immune cells. Surprisingly, although NK cells provide protection against T. cruzi, and are a major source of IFN-gamma following alpha-GalCer treatment, NK cells are not required for the alpha-GalCer-induced protection. The alpha-GalCer treatment of NK-cell-depleted mice controlled parasitaemia and prevented death. In contrast, phagocytes, helper T cells and cytotoxic T cells are required. Furthermore, alpha-GalCer treatment of MHC II-/- or CD8 alpha(-/-) mice exacerbated the infection, demonstrating that alpha-GalCer treatment induces some responses that favour the parasite. In summary alpha-GalCer protection against T. cruzi required multiple cellular responses, but not the response of NK cells. These results provide useful information because alpha-GalCer is being developed as therapy for infections, autoimmune diseases, allergy and cancers.
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