Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production

Myeloid differentiation factor-88 plays a crucial role in the pathogenesis of coxsackievirus B3-induced myocarditis and influences type I interferon production

Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown. We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-typ...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 2005-10, Vol.112 (15), p.2276-2285
Hauptverfasser: FUSE, Koichi, CHAN, Grace, YOUAN LIU, GUDGEON, Patrick, HUSAIN, Mansoor, MANYIN CHEN, YEH, Wen-Chen, AKIRA, Shizuo, LIU, Peter P
Format: Artikel
Sprache:eng
Schlagworte:
Adaptor Proteins, Signal Transducing - deficiency
Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - physiology
Animals
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Coronary heart disease
Coxsackievirus B3
Disease Models, Animal
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
DNA Primers
Drug toxicity and drugs side effects treatment
Enterovirus B, Human
Enterovirus Infections - complications
Enterovirus Infections - immunology
Heart
Heart - virology
HeLa Cells
Humans
Immunity, Innate
Inflammation - immunology
Inflammation - physiopathology
Interferon Type I - biosynthesis
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Myeloid Differentiation Factor 88
Myocarditis - immunology
Myocarditis - physiopathology
Myocarditis - virology
Pharmacology. Drug treatments
Reverse Transcriptase Polymerase Chain Reaction
Toxicity: blood
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Zusammenfassung:Myeloid differentiation factor (MyD)-88 is a key adaptor protein that plays a major role in the innate immune pathway. How MyD88 may regulate host response in inflammatory heart disease is unknown. We found that the cardiac protein level of MyD88 was significantly increased in the hearts of wild-type mice after exposure to Coxsackievirus B3 (CVB3). MyD88(-/-) mice showed a dramatic higher survival rate (86%) in contrast to the low survival (35%) in the MyD88(+/+) mice after CVB3 infection (P
ISSN:0009-7322
1524-4539
DOI:10.1161/CIRCULATIONAHA.105.536433