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

Authors

  • Olivier Joffre,

    1. Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln’s Inn Fields Laboratories, London, UK.
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      These authors contributed equally.

  • Martijn A. Nolte,

    1. Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
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      These authors contributed equally.

  • Roman Spörri,

    1. ETH Zürich, Institute for Microbiology, Zürich, Switzerland.
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      These authors contributed equally.

  • Caetano Reis e Sousa

    1. Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln’s Inn Fields Laboratories, London, UK.
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Caetano Reis e Sousa
Immunobiology Laboratory
Cancer Research UK
London Research Institute
Lincoln’s Inn Fields Laboratories
44 Lincoln’s Inn Fields
London WC2A 3PX, UK
Tel.: +44 20 7269 2832
Fax: +44 20 7269 2833
e-mail: caetano@cancer.org.uk

Abstract

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.

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