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.
Department of Microbiology, Immunology and Molecular Genetics, Medical Scientist Training Program, University of California at Los Angeles, Los Angeles, California 90095, USA.
Supriya K
SK
Saha
Genhong
G
Cheng
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