Author: Crane, Meredith J.; Gaddi, Pamela J.; Salazar-Mather, Thais P.
Title: UNC93B1 Mediates Innate Inflammation and Antiviral Defense in the Liver during Acute Murine Cytomegalovirus Infection Document date: 2012_6_18
ID: 0vsf67nh_1
Snippet: Initiation of inflammation following infection requires recognition of the invading microbe by innate immune pattern recognition receptors (PRRs) that signal in response to pathogen-associated molecular patterns (PAMPs). PRRs recognize selfand microbe-associated molecules [1] [2] [3] [4] . Members of the Toll-like receptor (TLR) family of PRRs are transmembrane receptors that are expressed either on the cell surface or within the endosomal compar.....
Document: Initiation of inflammation following infection requires recognition of the invading microbe by innate immune pattern recognition receptors (PRRs) that signal in response to pathogen-associated molecular patterns (PAMPs). PRRs recognize selfand microbe-associated molecules [1] [2] [3] [4] . Members of the Toll-like receptor (TLR) family of PRRs are transmembrane receptors that are expressed either on the cell surface or within the endosomal compartment and respond to a variety of PAMPs [1] . Murine TLR3, TLR7 and TLR9 are expressed in the endolysosome and are implicated in recognition of viral dsRNA, ssRNA and dsDNA, respectively [1, [5] [6] [7] [8] [9] [10] [11] . Ligation of the nucleic acid-sensing TLRs results in transcription of antiviral genes including type I IFNs (IFN-a/b) and proinflammatory cytokines [1] . TLR3 responses require signaling through the adaptor molecule Toll/IL-1R domain-containing adapter-inducing interferon-b (TRIF), while TLR7 and TLR9 are dependent on the adaptor molecule myeloid differentiation primary response gene 88 (MyD88) to activate transcription factors and induce gene transcription [1, [12] [13] [14] .
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