| First Author | Wang D | Year | 2019 |
| Journal | J Biol Chem | Volume | 294 |
| Issue | 19 | Pages | 7787-7796 |
| PubMed ID | 30898878 | Mgi Jnum | J:280508 |
| Mgi Id | MGI:6368310 | Doi | 10.1074/jbc.RA118.006321 |
| Citation | Wang D, et al. (2019) ELF4 facilitates innate host defenses against Plasmodium by activating transcription of Pf4 and Ppbp. J Biol Chem 294(19):7787-7796 |
| abstractText | Platelet factor 4 (PF4) is an anti-Plasmodium component of platelets. It is expressed in megakaryocytes and released from platelets following infection with Plasmodium Innate immunity is crucial for the host anti-Plasmodium response, in which type I interferon plays an important role. Whether there is cross-talk between innate immune signaling and the production of anti-Plasmodium defense peptides is unknown. Here we demonstrate that E74, like ETS transcription factor 4 (ELF4), a type I interferon activator, can help protect the host from Plasmodium yoelii infection. Mechanically, ELF4 binds to the promoter of genes of two C-X-C chemokines, Pf4 and pro-platelet basic protein (Ppbp), initiating the transcription of these two genes, thereby enhancing PF4-mediated killing of parasites from infected erythrocytes. Elf4 (-/-) mice are much more susceptible to Plasmodium infection than WT littermates. The expression level of Pf4 and Ppbp in megakaryocytes from Elf4 (-/-) mice is much lower than in those from control animals, resulting in increased parasitemia. In conclusion, our study uncovered a distinct role of ELF4, an innate immune molecule, in host defense against malaria. |
