HCFC2 is needed for IRF1- and IRF2-dependent Tlr3 transcription and for survival during viral infections.
J Exp Med
; 214(11): 3263-3277, 2017 Nov 06.
Article
en En
| MEDLINE
| ID: mdl-28970238
ABSTRACT
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(IC)) 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(IC) 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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Factores de Transcripción
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Factor 1 Regulador del Interferón
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Factor 2 Regulador del Interferón
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Receptor Toll-Like 3
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Macrófagos
Límite:
Animals
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Female
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Humans
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Male
Idioma:
En
Revista:
J Exp Med
Año:
2017
Tipo del documento:
Article