Abstract

Summary: The innate immune system detects viruses through molecular sensors that trigger the production of type I interferons (IFN-I) and inflammatory cytokines. As viruses vary tremendously in size, structure, genomic composition, and tissue tropism, multiple sensors are required to detect their presence in various cell types and tissues. In this review, we summarize current knowledge of the diversity, specificity, and signaling pathways downstream of viral sensors and ask whether two distinct sensors that recognize the same viral component are complementary, compensatory, or simply redundant. We also discuss why viral sensors are differentially distributed in distinct cell types and whether a particular cell type dominates the IFN-I response during viral infection. Finally, we review evidence suggesting that inappropriate signaling through viral sensors may induce autoimmunity. The picture emerging from these studies is that disparate viral sensors in different cell types form a dynamic and integrated molecular network that can be exploited for improving vaccination and therapeutic strategies for infectious and autoimmune diseases.

Original languageEnglish
Pages (from-to)74-90
Number of pages17
JournalImmunological Reviews
Volume243
Issue number1
DOIs
StatePublished - Sep 2011

Keywords

  • Autoimmunity
  • Dendritic cells
  • Diabetes
  • Systemic lupus erythematosus
  • Toll-like receptors/pattern recognition receptors
  • Virus

Fingerprint

Dive into the research topics of 'dsRNA sensors and plasmacytoid dendritic cells in host defense and autoimmunity'. Together they form a unique fingerprint.

Cite this