TRAF3: a new regulator of type I interferons.
Type I interferons are a major and essential component of the mammalian antiviral response. While many cell types produce type I interferons following viral infection, how cells detect the virus has remained a mystery for many years. Recently, multiple genome-encoded viral recognition receptors have been identified. Interestingly, all of the major viral recognition pathways characterized thus far require TRAF3 to initiate type I interferon production. In this review, we comment on the mechanistic and biological implications for the new role of TRAF3 in innate antiviral immunity.
Saha
Supriya K
SK
Department of Microbiology, Immunology and Molecular Genetics, Medical Scientist Training Program, University of California at Los Angeles, Los Angeles, California 90095, USA.
Cheng
Genhong
G
D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000818:Animals; D005786:Gene Expression Regulation; D016678:Genome; D006801:Humans; D007113:Immunity, Innate; D007370:Interferon Type I / Q000502:physiology*; D051379:Mice; D008954:Models, Biological; D053594:Myeloid Differentiation Factor 88; D048008:TNF Receptor-Associated Factor 3 / Q000378:metabolism / Q000502:physiology*; D051193:Toll-Like Receptors / Q000378:metabolism; D014777:Virus Diseases / Q000276:immunology*
D048868:Adaptor Proteins, Signal Transducing; D007370:Interferon Type I; C507779:MYD88 protein, human; C507780:Myd88 protein, mouse; D053594:Myeloid Differentiation Factor 88; D048008:TNF Receptor-Associated Factor 3; D051193:Toll-Like Receptors