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            <funder>This work was supported by institutional grants from the Curie Institute, INSERM, CNRS and by specific grants from Agence Nationale de la Recherche (ANR MECANOCAV-12-BSV2-0011 to C.L.), Institut National du Cancer (INCa PLBIO12-203 to C.L.), Marie Curie Actions–Networks for Initial Training (FP7-PEOPLE-2010-ITN to C.L. and D.C.), Fondation pour la Recherche Médicale to D.C. and DFG (SFB 944) to S.W. and J.P. The Johannes and Lamaze teams are members of Labex CelTisPhyBio Number ANR-10-LBX-0038 and part of the IDEX Idex PSL Number ANR-10-IDEX-0001-02 PSL.</funder>
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              <p>Type-I interferons (IFNs) play a key role in the immune defences against viral and bacterial infections, and in cancer immunosurveillance. We have established that clathrin-dependent endocytosis of the type-I interferon (IFN-α/β) receptor (IFNAR) is required for JAK/STAT signalling. Here we show that the internalized IFNAR1 and IFNAR2 subunits of the IFNAR complex are differentially sorted by the retromer at the early endosome. Binding of the retromer VPS35 subunit to IFNAR2 results in IFNAR2 recycling to the plasma membrane, whereas IFNAR1 is sorted to the lysosome for degradation. Depletion of VPS35 leads to abnormally prolonged residency and association of the IFNAR subunits at the early endosome, resulting in increased activation of STAT1- and IFN-dependent gene transcription. These experimental data establish the retromer complex as a key spatiotemporal regulator of IFNAR endosomal sorting and a new factor in type-I IFN-induced JAK/STAT signalling and gene transcription.</p>
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