Homeostatic NF-κB Signaling in Steady-State Migratory Dendritic Cells Regulates Immune Homeostasis and Tolerance

Myriam Baratin, Chloe Foray, Olivier Demaria, Mohamed Habbeddine, Emeline Pollet, Julien Maurizio, Christophe Verthuy, Suzel Davanture, Hiroaki Azukizawa, Adriana Flores-Langarica, Marc Dalod, Toby Lawrence

    Research output: Contribution to journalArticlepeer-review

    74 Citations (Scopus)
    67 Downloads (Pure)


    Migratory non-lymphoid tissue dendritic cells (NLT-DCs) transport antigens to lymph nodes (LNs) and are required for protective immune responses in the context of inflammation and to promote tolerance to self-antigens in steady-state. However, the molecular mechanisms that elicit steady-state NLT-DC maturation and migration are unknown. By comparing the transcriptome of NLT-DCs in the skin with their migratory counterparts in draining LNs, we have identified a novel NF-κB-regulated gene network specific to migratory DCs. We show that targeted deletion of IKKβ in DCs, a major activator of NF-κB, prevents NLT-DC accumulation in LNs and compromises regulatory T cell conversion in vivo. This was associated with impaired tolerance and autoimmunity. NF-κB is generally considered the prototypical pro-inflammatory transcription factor, but this study describes a role for NF-κB signaling in DCs for immune homeostasis and tolerance that could have implications in autoimmune diseases and immunity.

    Original languageEnglish
    Pages (from-to)627-639
    Number of pages13
    Issue number4
    Early online date7 Apr 2015
    Publication statusPublished - 21 Apr 2015


    • Animals
    • Autoantigens
    • Autoimmunity
    • Cell Movement
    • Dendritic Cells
    • Gene Expression Profiling
    • Gene Expression Regulation
    • Gene Regulatory Networks
    • Homeostasis
    • I-kappa B Kinase
    • Immune Tolerance
    • Lymph Nodes
    • Mice
    • Mice, Knockout
    • Microarray Analysis
    • NF-kappa B
    • Signal Transduction
    • Skin
    • Spleen
    • T-Lymphocytes, Regulatory
    • Journal Article
    • Research Support, Non-U.S. Gov't


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