The MyD88 Pathway in Plasmacytoid and CD4+ Dendritic Cells Primarily Triggers Type I IFN Production against Measles Virus in a Mouse Infection Model

• Published in: The Journal of immunology (1950) Vol. 191; no. 9; pp. 4740 - 4747
• Main Authors: Takaki, Hiromi, Takeda, Makoto, Tahara, Maino, Shingai, Masashi, Oshiumi, Hiroyuki, Matsumoto, Misako, Seya, Tsukasa
• Format: Journal Article
• Language: English
• Published: United States 01.11.2013
• Subjects: Adaptor Proteins, Signal Transducing - biosynthesis; Adaptor Proteins, Signal Transducing - genetics; Animals; Antigens, CD - biosynthesis; Antigens, CD - metabolism; B-Lymphocytes - immunology; CD4 Antigens - metabolism; CD8 Antigens - metabolism; Cells, Cultured; Dendritic Cells - immunology; Dendritic Cells - metabolism; Disease Models, Animal; Humans; Interferon Type I - biosynthesis; Measles - immunology; Measles - virology; Measles virus; Measles virus - immunology; Mice; Mice, Inbred C57BL; Mice, Knockout; Myeloid Differentiation Factor 88 - metabolism; Receptor, Interferon alpha-beta - biosynthesis; Receptor, Interferon alpha-beta - genetics; Receptors, Cell Surface - biosynthesis; Receptors, Cell Surface - metabolism; Signaling Lymphocytic Activation Molecule Family Member 1; Spleen - cytology; T-Lymphocytes - immunology

Infection by measles virus (MV) induces type I IFN via the retinoic acid–inducible gene I/melanoma differentiation–associated gene 5/mitochondrial antiviral signaling protein (MAVS) pathway in human cells. However, the in vivo role of the MAVS pathway in host defense against MV infection remains und...