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            <funder>Funding: This work was supported by Labex EpiGenMed, an Investissements d’avenir program (ANR-10-LABX-12-01 to N.J.A. and S.N.); the Agence National de la Recherche sur le SIDA et les Hépatites virales, ANRS (AO2017-1 to J.-P.H.); the European Community’s Seventh Framework Program (FP7- PEOPLE-2011-ITN) under the Marie-Curie Initial Training Network FishForPharma (PITN-GA-2011-289209 to G.L.); the European Community’s H2020 Program Marie-Curie Innovative Training Network ImageInLife (721537 to G.L. and J.-P.L.); the Agence Nationale de la Recherche (ANR-16-CE20-0002-03 and ANR-10-MDI-009 to J.-P.L.); and the Région Occitanie (REPERE2017ImageInLife to G.L.). G.M. (AO2018-2), N.S. (AO2016-1), O.M. (AO2017-1), and S.M. (AO2017-2) were supported by grants from the ANRS. This work received help and expertise from TACGene, which is supported by the program Investissement d’avenir TEFOR (ANR-II-INSB-0014). N.S. acknowledges support from the European Molecular Biology Organization EMBO for Fellowship (LT-834-2017), the start-up funding program “Baustein” of the Medical Faculty of Ulm University (LSBN.0147), and the Deutsche Forschungsgemeinschaft DFG (SM 544/1-1).</funder>
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              <p>Plasmacytoid dendritic cells (pDCs) play a crucial role in antiviral innate immunity through their unique capacity to produce large amounts of type I interferons (IFNs) upon viral detection. Tripartite motif (TRIM) proteins have recently come forth as important modulators of innate signaling, but their involvement in pDCs has not been investigated. Here, we performed a rationally streamlined small interfering RNA (siRNA)-based screen of TRIM proteins in human primary pDCs to identify those that are critical for the IFN response. Among candidate hits, TRIM8 emerged as an essential regulator of IFN regulatory factor 7 (IRF7) function. Mechanistically, TRIM8 protects phosphorylated IRF7 (pIRF7) from proteasomal degradation in an E3 ubiquitin ligase-independent manner by preventing its recognition by the peptidyl-prolyl isomerase Pin1. Our findings uncover a previously unknown regulatory mechanism of type I IFN production in pDCs by which TRIM8 and Pin1 oppositely regulate the stability of pIRF7.</p>
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