Increased expression with differential subcellular location of cytidine deaminase APOBEC3G in human CD4+ T-cell activation and dendritic cell maturation

Harold Oliva, Rodrigo Pacheco, José M. Martinez-Navio, Marta Rodríguez-García, Mar Naranjo-Gómez, Núria Climent, Carolina Prado, Cristina Gil, Montserrat Plana, Felipe García, José M. Miró, Rafael Franco, Francesc E. Borras, Naveenan Navaratnam, José M. Gatell, Teresa Gallart

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    5 Citations (Scopus)

    Abstract

    © 2016 Australasian Society for Immunology Inc. All rights reserved. APOBEC3G (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G; A3G) is an innate defense protein showing activity against retroviruses and retrotransposons. Activated CD4+ T cells are highly permissive for HIV-1 replication, whereas resting CD4+ T cells are refractory. Dendritic cells (DCs), especially mature DCs, are also refractory. We investigated whether these differences could be related to a differential A3G expression and/or subcellular distribution. We found that A3G mRNA and protein expression is very low in resting CD4+ T cells and immature DCs, but increases strongly following T-cell activation and DC maturation. The Apo-7 anti-A3G monoclonal antibody (mAb), which was specifically developed, confirmed these differences at the protein level and disclosed that A3G is mainly cytoplasmic in resting CD4+ T cells and immature DCs. Nevertheless, A3G translocates to the nucleus in activated-proliferating CD4+ T cells, yet remaining cytoplasmic in matured DCs, a finding confirmed by immunoblotting analysis of cytoplasmic and nuclear fractions. Apo-7 mAb was able to immunoprecipitate endogenous A3G allowing to detect complexes with numerous proteins in activated-proliferating but not in resting CD4+ T cells. The results show for the first time the nuclear translocation of A3G in activated-proliferating CD4+ T cells.
    Original languageEnglish
    Pages (from-to)689-700
    JournalImmunology and Cell Biology
    Volume94
    Issue number7
    DOIs
    Publication statusPublished - 1 Aug 2016

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