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Sharma, Shruti; DeOliveira, Rosane B.; Kalantari, Parisa; Parroche, Peggy; Goutagny, Nadege; Jiang, Zhaozhao; Chan, Jennie; Bartholomeu, Daniella C.; Lauw, Fanny; Hall, J. Perry; Barber, Glen N.; Gazzinelli, Ricardo T.; Fitzgerald, Katherine A.; Golenbock, Douglas T.
Immunity (Cambridge, Mass.), 08/2011, Letnik: 35, Številka: 2Journal Article
Although Toll-like receptor 9 (TLR9) has been implicated in cytokine and type I interferon (IFN) production during malaria in humans and mice, the high AT content of the Plasmodium falciparum genome prompted us to examine the possibility that malarial DNA triggered TLR9-independent pathways. Over 6000 ATTTTTAC (“AT-rich”) motifs are present in the genome of P. falciparum, which we show here potently induce type I IFNs. Parasite DNA, parasitized erythrocytes and oligonucleotides containing the AT-rich motif induce type I IFNs via a pathway that did not involve the previously described sensors TLR9, DAI, RNA polymerase-III or IFI16/p204. Rather, AT-rich DNA sensing involved an unknown receptor that coupled to the STING, TBK1 and IRF3-IRF7 signaling pathway. Mice lacking IRF3, IRF7, the kinase TBK1 or the type I IFN receptor were resistant to otherwise lethal cerebral malaria. Collectively, these observations implicate AT-rich DNA sensing via STING, TBK1 and IRF3-IRF7 in P. falciparum malaria. ► Plasmodium falciparum induces type I IFN inducible genes during infections ► Pf genomic DNA is AT rich and induces type I IFNs in a TLR9-independent manner ► Pf AT-rich DNA triggers a STING-dependent DNA sensing pathway ► Malarial pathology involves TBK1 and IRF3-IRF7-dependent production of type I IFNs
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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