期刊
JOURNAL OF IMMUNOLOGY
卷 200, 期 4, 页码 1243-1248出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701010
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资金
- National Institutes of Health [R01AI079293, R01NS098747, U19AI0089681, T32AI095213, R01AI095192, R01AI130131]
- European Research Council [310372]
- Netherlands Organization for Scientific Research
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R21AI131632, P30AI036219, R01AI130131, T32AI095213, R01AI079293, U19AI089681, R01AI095192, R37AI067497] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS098747] Funding Source: NIH RePORTER
Malarial infection in naive individuals induces a robust innate immune response. In the recently described model of innate immune memory, an initial stimulus primes the innate immune system to either hyperrespond (termed training) or hyporespond (tolerance) to subsequent immune challenge. Previous work in both mice and humans demonstrated that infection with malaria can both serve as a priming stimulus and promote tolerance to subsequent infection. In this study, we demonstrate that initial stimulation with Plasmodium falciparum-infected RBCs or the malaria crystal hemozoin induced human adherent PBMCs to hyperrespond to subsequent ligation of TLR2. This hyperresponsiveness correlated with increased H3K4me3 at important immunometabolic promoters, and these epigenetic modifications were also seen in Kenyan children naturally infected with malaria. However, the use of epigenetic and metabolic inhibitors indicated that the induction of trained immunity by malaria and its ligands may occur via a previously unrecognized mechanism(s).
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