Role of Toll like receptor-activated dendritic cells in the development of autoimmunity

Francesca Granucci, Ivan Zanoni

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The recognition of microbial stimuli by Toll-like receptors (TLRs) expressed on dendritic cells (DCs) is essential for the regulation of immune responses. DC activation via TLRs leads to the production of proinflammatory cytokines, chemokines and surface molecules that play a key role in the regulation and control of inflammatory reactions and adaptive immunity. Minor imbalances in the feedback control of TLR-activated innate immune cells have been associated with autoimmunity in genetically prone individuals. We review here recent studies indicating how TLR-mediated activation of innate immune cells, including DCs, may be involved in the development and/or maintenance of autoimmune responses in the presence of both endogenous and exogenous ligands.

Original languageEnglish
Pages (from-to)4817-4826
Number of pages10
JournalFrontiers in Bioscience
Volume13
Issue number13
DOIs
Publication statusPublished - 2008

Fingerprint

Toll-Like Receptors
Autoimmunity
Dendritic Cells
Chemical activation
Adaptive Immunity
Chemokines
Feedback control
Maintenance
Cytokines
Ligands
Molecules

Keywords

  • Autoimmunity
  • Dendritic cells
  • Endogenous toll-like receptor ligands
  • Exogenous toll-like receptor ligands
  • Review
  • Toll-like receptors
  • Type I interferons

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Role of Toll like receptor-activated dendritic cells in the development of autoimmunity. / Granucci, Francesca; Zanoni, Ivan.

In: Frontiers in Bioscience, Vol. 13, No. 13, 2008, p. 4817-4826.

Research output: Contribution to journalArticle

Granucci, Francesca ; Zanoni, Ivan. / Role of Toll like receptor-activated dendritic cells in the development of autoimmunity. In: Frontiers in Bioscience. 2008 ; Vol. 13, No. 13. pp. 4817-4826.
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