These authors contributed equally.
Inflammatory signals in dendritic cell activation and the induction of adaptive immunity
Version of Record online: 19 DEC 2008
© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard
Special Issue: Innate Recognition: Receptors & Signaling
Volume 227, Issue 1, pages 234–247, January 2009
How to Cite
Joffre, O., Nolte, M. A., Spörri, R. and Sousa, C. R. e. (2009), Inflammatory signals in dendritic cell activation and the induction of adaptive immunity. Immunological Reviews, 227: 234–247. doi: 10.1111/j.1600-065X.2008.00718.x
- Issue online: 19 DEC 2008
- Version of Record online: 19 DEC 2008
- dendritic cells;
- T cells;
- pattern recognition receptors;
Summary: Pathogen invasion induces a rapid inflammatory response initiated through the recognition of pathogen-derived molecules by pattern recognition receptors (PRRs) expressed on both immune and non-immune cells. The initial wave of pro-inflammatory cytokines and chemokines limits pathogen spread and recruits and activates immune cells to eradicate the invaders. Dendritic cells (DCs) are responsible for initiating a subsequent phase of immunity, dominated by the action of pathogen-specific T and B cells. As for the early pro-inflammatory response, DC activation is triggered by PRR signals. These signals convert resting DCs into potent antigen-presenting cells capable of promoting the expansion and effector differentiation of naive pathogen-specific T cells. However, it has been argued that signals from PRRs are not a prerequisite for DC activation and that pro-inflammatory cytokines have the same effect. Although this may appear like an efficient way to expand the number of DCs that initiate adaptive immunity, evidence is accumulating that DCs activated indirectly by inflammatory cytokines are unable to induce functional T-cell responses. Here, we review the differences between PRR-triggered and cytokine-induced DC activation and speculate on a potential role for DCs activated by inflammatory signals in tolerance induction rather than immunity.