PMID- 22345444 OWN - NLM STAT- MEDLINE DCOM- 20120618 LR - 20211021 IS - 1098-5514 (Electronic) IS - 0022-538X (Print) IS - 0022-538X (Linking) VI - 86 IP - 9 DP - 2012 May TI - Measles virus glycoprotein-pseudotyped lentiviral vectors are highly superior to vesicular stomatitis virus G pseudotypes for genetic modification of monocyte-derived dendritic cells. PG - 5192-203 LID - 10.1128/JVI.06283-11 [doi] AB - Dendritic cells (DCs) are potent antigen-presenting cells capable of promoting or regulating innate and adaptive immune responses against non-self antigens. To better understand the DC biology or to use them for immune intervention, a tremendous effort has been made to improve gene transfer in these cells. Lentiviral vectors (LVs) have conferred a huge advantage in that they can transduce nondividing cells such as human monocyte-derived DCs (MDDCs) but required high amounts of viral particles and/or accessory proteins such as Vpx or Vpr to achieve sufficient transduction rates. As a consequence, these LVs have been shown to cause dramatic functional modifications, such as the activation or maturation of transduced MDDCs. Taking advantage of new pseudotyped LVs, i.e., with envelope glycoproteins from the measles virus (MV), we demonstrate that MDDCs are transduced very efficiently with these new LVs compared to the classically used vesicular stomatitis virus G-pseudotyped LVs and thus allowed to achieve high transduction rates at relatively low multiplicities of infection. Moreover, in this experimental setting, no activation or maturation markers were upregulated, while MV-LV-transduced cells remained able to mature after an appropriate Toll-like receptor stimulation. We then demonstrate that our MV-pseudotyped LVs use DC-SIGN, CD46, and CD150/SLAM as receptors to transduce MDDCs. Altogether, our results show that MV-pseudotyped LVs provide the most accurate and simple viral method for efficiently transferring genes into MDDCs without affecting their activation and/or maturation status. FAU - Humbert, J-M AU - Humbert JM AD - INSERM UMR643-Institute for Transplantation, Urology, and Nephrology, Nantes, France. FAU - Frecha, C AU - Frecha C FAU - Amirache Bouafia, F AU - Amirache Bouafia F FAU - N'Guyen, T H AU - N'Guyen TH FAU - Boni, S AU - Boni S FAU - Cosset, F-L AU - Cosset FL FAU - Verhoeyen, E AU - Verhoeyen E FAU - Halary, F AU - Halary F LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120215 PL - United States TA - J Virol JT - Journal of virology JID - 0113724 RN - 0 (Cell Adhesion Molecules) RN - 0 (DC-specific ICAM-3 grabbing nonintegrin) RN - 0 (Lectins, C-Type) RN - 0 (Membrane Cofactor Protein) RN - 0 (Receptors, Cell Surface) RN - 0 (Toll-Like Receptor 3) RN - 0 (Viral Envelope Proteins) SB - IM MH - Cell Adhesion Molecules/genetics MH - Cell Differentiation MH - Dendritic Cells/cytology/*metabolism/virology MH - Gene Expression MH - Gene Transfer Techniques MH - Genetic Vectors/*genetics MH - Humans MH - Lectins, C-Type/genetics MH - Lentivirus/*genetics MH - Measles virus/*genetics MH - Membrane Cofactor Protein/genetics MH - Receptors, Cell Surface/genetics MH - Resting Phase, Cell Cycle MH - Toll-Like Receptor 3/agonists MH - *Transduction, Genetic MH - Vesicular stomatitis Indiana virus/*genetics MH - Viral Envelope Proteins/*genetics PMC - PMC3347358 EDAT- 2012/02/22 06:00 MHDA- 2012/06/19 06:00 PMCR- 2012/11/01 CRDT- 2012/02/21 06:00 PHST- 2012/02/21 06:00 [entrez] PHST- 2012/02/22 06:00 [pubmed] PHST- 2012/06/19 06:00 [medline] PHST- 2012/11/01 00:00 [pmc-release] AID - JVI.06283-11 [pii] AID - 06283-11 [pii] AID - 10.1128/JVI.06283-11 [doi] PST - ppublish SO - J Virol. 2012 May;86(9):5192-203. doi: 10.1128/JVI.06283-11. Epub 2012 Feb 15.