期刊
CELL REPORTS
卷 7, 期 2, 页码 436-447出版社
CELL PRESS
DOI: 10.1016/j.celrep.2014.03.018
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资金
- Bill and Melinda Gates Foundation [OPP1016829]
- Bill and Melinda Gates Foundation [OPP1016829] Funding Source: Bill and Melinda Gates Foundation
Mosquito-transmitted malaria parasites infect hepatocytes and asymptomatically replicate as liver stages. Using RNA sequencing, we show that a rodent malaria liver-stage infection stimulates a robust innate immune response including type I interferon (IFN) and IFN gamma pathways. Liver-stage infection is suppressed by these infection-engendered innate responses. This suppression was abrogated in mice deficient in IFNg, the type I IFN alpha/beta receptor (IFNAR), and interferon regulatory factor 3. Natural killer and CD49b(+) CD3(+) natural killer T (NKT) cells increased in the liver after a primary infection, and CD1d-restricted NKT cells, which secrete IFN gamma, were critical in reducing liver-stage burden of a secondary infection. Lack of IFNAR signaling abrogated the increase in NKT cell numbers in the liver, showing a link between type I IFN signaling, cell recruitment, and subsequent parasite elimination. Our findings demonstrate innate immune sensing of malaria parasite liver-stage infection and that the ensuing innate responses can eliminate the parasite.
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