We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Autocrine Type I Interferon Amplifies Dendritic Cell Responses to Lipopolysaccharide via the Nuclear Factor-κB/p38 Pathways.
- Authors
Pollara, G.; Handley, M. E.; Kwan, A.; Chain, B. M.; Katz, D. R.
- Abstract
The central role of dendritic cells (DC) in the initiation of immune responses requires these cells to be able to determine the degree of danger in their microenvironment. Abrogating the activity of type I interferon (IFN) secreted after lipopolysaccharide (LPS) stimulation of DC inhibits CD86 and human leucocyte antigen-DR (HLA-DR) upregulation at a low LPS concentration. At a higher concentration of LPS, while changes in surface phenotype are not dependent on type I IFN, this cytokine is required for maximal secretion of interleukin-12 (IL-12) and tumour necrosis factor-α (TNFα) by DC. Thus, the secretion and autocrine activity of type I IFN after Toll-like receptor stimulation enables DC to orchestrate a hierarchical maturation response with regard to changes in surface phenotype and secretion of cytokines. In addition, the activation of nuclear factor-κB and p38 pathways in DC can occur either in an additive fashion when DC are exposed to dual stimulation or can be activated in discrete phases over time when DC are exposed to LPS alone. The differential activation of these pathways provides a mechanism for DC to integrate the activation by multiple stimuli and thus amplify responses to pathogen infection.
- Subjects
INTERFERONS; DENDRITIC cells; IMMUNOREGULATION; ENDOTOXINS; PATHOGENIC microorganisms; AUTOCRINE mechanisms; GENOTYPE-environment interaction; CELLULAR immunity
- Publication
Scandinavian Journal of Immunology, 2006, Vol 63, Issue 3, p151
- ISSN
0300-9475
- Publication type
Article
- DOI
10.1111/j.1365-3083.2006.01727.x