The Vici syndrome protein EPG5 regulates intracellular nucleic acid trafficking linking autophagy to innate and adaptive immunity

E. Piano Mortari, V. Folgiero, V. Marcellini, P. Romania, E. Bellacchio, V. D'Alicandro, C. Bocci, R. Carrozzo, D. Martinelli, S. Petrini, E. Axiotis, C. Farroni, F. Locatelli, U. Schara, D.T. Pilz, H. Jungbluth, C. Dionisi-Vici & R. Carsetti
Vici syndrome is a human inherited multi-system disorder caused by recessive mutations in EPG5, encoding the EPG5 protein that mediates the fusion of autophagosomes with lysosomes. Immunodeficiency characterized by lack of memory B cells and increased susceptibility to infection is an integral part of the condition, but the role of EPG5 in the immune system remains unknown. Here we show that EPG5 is indispensable for the transport of the TLR9 ligand CpG to the late...
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