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• W2802903012 abstract "Dendritic cells (DC) and cytokines produced by DC play crucial roles in inducing and regulating pro-/anti-inflammatory and Th1/Th2 responses. DC are known to produce a Th1-promoting cytokine, interleukin (IL)-12, in response to malaria and other pathogenic infections, but it is thought that DC do not produce Th2-promoting cytokine, IL-4. Here, we show that a protein factor of malaria parasites induces IL-4 responses by CD11chiMHCIIhiCD3ϵ−CD49b−CD19−FcϵRI− DC via PI3K–Akt–NF-κB signaling independent of TLR-MyD88/TRIF. Malaria parasite–activated DC induced IL-4 responses by T cells both in vitro and in vivo, favoring Th2, and il-4–deficient DC were unable to induce IL-4 expression by T cells. Interestingly, lethal parasites, Plasmodium falciparum and Plasmodium berghei ANKA, induced IL-4 response primarily by CD8α− DC, whereas nonlethal Plasmodium yoelii induced IL-4 by both CD8α+ and CD8α− DC. In both P. berghei ANKA- and P. yoelii-infected mice, IL-4–expressing CD8α− DC did not express IL-12, but a distinct CD8α− DC subset expressed IL-12. In P. berghei ANKA infection, CD8α+ DC expressed IL-12 but not IL-4, whereas in P. yoelii infection, CD8α+ DC expressed IL-4 but not IL-12. These differential IL-4 and IL-12 responses by DC subsets may contribute to different Th1/Th2 development and clinical outcomes in lethal and nonlethal malaria. Our results for the first time demonstrate that a malaria protein factor induces IL-4 production by DC via PI3K–Akt–NF-κB signaling, revealing signaling and molecular mechanisms that initiate and promote Th2 development. Dendritic cells (DC) and cytokines produced by DC play crucial roles in inducing and regulating pro-/anti-inflammatory and Th1/Th2 responses. DC are known to produce a Th1-promoting cytokine, interleukin (IL)-12, in response to malaria and other pathogenic infections, but it is thought that DC do not produce Th2-promoting cytokine, IL-4. Here, we show that a protein factor of malaria parasites induces IL-4 responses by CD11chiMHCIIhiCD3ϵ−CD49b−CD19−FcϵRI− DC via PI3K–Akt–NF-κB signaling independent of TLR-MyD88/TRIF. Malaria parasite–activated DC induced IL-4 responses by T cells both in vitro and in vivo, favoring Th2, and il-4–deficient DC were unable to induce IL-4 expression by T cells. Interestingly, lethal parasites, Plasmodium falciparum and Plasmodium berghei ANKA, induced IL-4 response primarily by CD8α− DC, whereas nonlethal Plasmodium yoelii induced IL-4 by both CD8α+ and CD8α− DC. In both P. berghei ANKA- and P. yoelii-infected mice, IL-4–expressing CD8α− DC did not express IL-12, but a distinct CD8α− DC subset expressed IL-12. In P. berghei ANKA infection, CD8α+ DC expressed IL-12 but not IL-4, whereas in P. yoelii infection, CD8α+ DC expressed IL-4 but not IL-12. These differential IL-4 and IL-12 responses by DC subsets may contribute to different Th1/Th2 development and clinical outcomes in lethal and nonlethal malaria. Our results for the first time demonstrate that a malaria protein factor induces IL-4 production by DC via PI3K–Akt–NF-κB signaling, revealing signaling and molecular mechanisms that initiate and promote Th2 development." @default.
• W2802903012 created "2018-05-17" @default.
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• W2802903012 date "2018-07-01" @default.
• W2802903012 modified "2023-09-29" @default.
• W2802903012 title "A malaria protein factor induces IL-4 production by dendritic cells via PI3K–Akt–NF-κB signaling independent of MyD88/TRIF and promotes Th2 response" @default.
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• W2802903012 doi "https://doi.org/10.1074/jbc.ac118.001720" @default.
• W2802903012 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6036203" @default.
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