| First Author | Sun L | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 11 | Pages | 3263-3277 |
| PubMed ID | 28970238 | Mgi Jnum | J:251008 |
| Mgi Id | MGI:5923623 | Doi | 10.1084/jem.20161630 |
| Citation | Sun L, et al. (2017) HCFC2 is needed for IRF1- and IRF2-dependent Tlr3 transcription and for survival during viral infections. J Exp Med 214(11):3263-3277 |
| abstractText | Transcriptional regulation of numerous interferon-regulated genes, including Toll-like receptor 3 (Tlr3), which encodes an innate immune sensor of viral double-stranded RNA, depends on the interferon regulatory factor 1 (IRF1) and IRF2 transcription factors. We detected specific abrogation of macrophage responses to polyinosinic-polycytidylic acid (poly(I:C)) resulting from three independent N-ethyl-N-nitrosourea-induced mutations in host cell factor C2 (Hcfc2). Hcfc2 mutations compromised survival during influenza virus and herpes simplex virus 1 infections. HCFC2 promoted the binding of IRF1 and IRF2 to the Tlr3 promoter, without which inflammatory cytokine and type I IFN responses to the double-stranded RNA analogue poly(I:C) are reduced in mouse macrophages. HCFC2 was also necessary for the transcription of a large subset of other IRF2-dependent interferon-regulated genes. Deleterious mutations of Hcfc2 may therefore increase susceptibility to diverse infectious diseases. |
