Inflammatory signals in dendritic cell activation and the induction of adaptive immunity

• Published in: Immunological reviews 2009-01, Vol.227 (1), p.234-247
• Main Authors: Joffre, Olivier, Nolte, Martijn A, Spörri, Roman, Sousa, Caetano Reis e
• Format: Article
• Language: English
• Subjects: Animals; Cell Differentiation - immunology; Cross-Priming - immunology; Cytokines - genetics; Cytokines - immunology; Cytokines - metabolism; Cytotoxicity, Immunologic - genetics; Cytotoxicity, Immunologic - immunology; dendritic cells; Dendritic Cells - immunology; Dendritic Cells - metabolism; Dendritic Cells - pathology; Immune Tolerance - immunology; Immunity, Cellular; Immunity, Innate; inflammation; Inflammation Mediators - immunology; Inflammation Mediators - metabolism; Lymphocyte Activation - immunology; Mice; pattern recognition receptors; Receptors, Pattern Recognition - genetics; Receptors, Pattern Recognition - immunology; Receptors, Pattern Recognition - metabolism; Signal Transduction - immunology; T cells; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - metabolism; T-Lymphocyte Subsets - pathology; T-lymphocytes; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; T-Lymphocytes - pathology; Transcriptional Activation - genetics; Transcriptional Activation - immunology
• ISSN: 0105-2896; 1600-065X
• DOI: 10.1111/j.1600-065X.2008.00718.x

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.