Lockable End zitierf compatibility available file, see jimmunol be found. 1This work was supported by the National Institute of Allergy and Infectious Diseases grant U54 AI057153 supported, R21 A1076975, A1007528 T32, ZSTK474 475110-96-4 and the National Institute of General Medical Sciences grant T32 GM007863. 2Address correspondence with Dr. David J. Miller, Department of Internal Medicine, Division of Infectious Diseases, 3560B MSRB II, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-5688. Phone: 763-0565. Fax: 615-5534. milldaviumich. NIH Public Access Author Manuscript J Immunol. Author manuscript, increases available in PMC 15th June 2011. Ver published in its final form, as follows: J Immunol. 15th June 2010, 184: 021 7010 �. doi: 10.4049/jimmunol.0904133.
NIH-PA Author Manuscript NIH-PA Author Manuscript ZSTK474 PI3K inhibitor NIH-PA Author Manuscript introduction of innate immune pathways important answers to the start contr The excitation and pattern recognition receptors of acids, the ligands that bind pathogens or activated dangerassociated molecular models, GE changed Or carbohydrate structures of nucleic. For antiviral innate immune response ligation of these receptors causes a cascade of signal transduction, leading to the production of IFN type I, other cytokines and cellular factors required for the generation of an antiviral micro cell. In addition, the antiviral PRR signaling for activating an appropriate adaptive immune response that is for the m Possible release of several viral infections important.
How to play the PRR-mediated signaling through innate immune system Insert the key into the F Promotion quickly, but non-specific antiviral activity of t, while delivering activation signals to produce st Amplifier specialized immune adaptive responses. There are three general steps innate antiviral immune response: activation, amplification and effector rkung production. Antiviral PRR is signaling by a variety of receptors, including normal transmembrane proteins TLR 2, 3, 4, 7/8 and 9, and introduced cytoplasmic retinoblastoma gene The inducible S Acid-I- Similar receptors RIG-I and melanoma associated with differential gene with 5. TLR3, TLR7 / 8 and TLR9 Recogn Not themselves nucleic Urefragmente of dsRNA and ssRNA hypomethylated CpG DNA, respectively BE, w During TLR4 Recogn t viral glycoproteins, and the viral ligand for TLR2 remains to be identified.
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Activated B and NF IRF3 κ hen nachtr Possible to obtained, The expression of many genes, the confinement for the assembly of a robust antiviral response, Lich type I IFN, induce either a paracrine or autocrine IFN-stimulated genes function response elements contain in their promoters IFNstimulated. There are several IFN-stimulated genes directly as antiviral effectors, but many are also members of the PRR antiviral pathways that a regulatory mechanism of positive feedback and amplification offers Rkung. The molecular mechanisms of antiviral signaling PRR were primarily using a limited number of cell lines and primary Rzellen cell types, including many models from small rodents and defined professional immune cells such as dendritic cells or macrophages. These studies have revealed significant cell type-specific differences in the kind of anti-viral PRR. For example, dendritic