Efficient inhibition of HIV-1 replication in human immature monocyte-derived dendritic cells by purified anti–HIV-1 IgG without induction of maturation

• Published in: Blood Vol. 107; no. 11; pp. 4466 - 4474
• Main Authors: Holl, Vincent, Peressin, Maryse, Schmidt, Sylvie, Decoville, Thomas, Zolla-Pazner, Susan, Aubertin, Anne-Marie, Moog, Christiane
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01.06.2006; The Americain Society of Hematology; The American Society of Hematology
• Subjects: Biological and medical sciences; Cell Differentiation; Cells, Cultured; Dendritic Cells - virology; Gene Expression Regulation - drug effects; HIV Antibodies - pharmacology; HIV Infections - prevention & control; HIV Infections - transmission; HIV-1 - physiology; Human viral diseases; Humans; Immunobiology; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunoglobulin G; Immunopathology; Infectious diseases; Interferon-gamma - pharmacology; Medical sciences; Receptors, IgG - genetics; Receptors, IgG - physiology; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Virus Replication; Human; Immunopathology; Dendritic cell; Monocyte; HIV-1 virus; Retroviridae; IgG; AIDS; Immune deficiency; Lentivirus; Infection; Virus; Prevention; Antigen presenting cell; Viral disease; Antiviral; Replication; Inhibitor; Human immunodeficiency virus; Immaturity
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood-2005-08-3490

During mucosal HIV transmission, immature dendritic cells (DCs) present in the mucosa are among the first cellular targets of the virus. Previous studies have analyzed the inhibition of HIV-1 transfer from human mature DCs to T lymphocytes by neutralizing IgG, but so far no in vitro data regarding the capacity of antibodies to inhibit HIV-1 infection of immature DCs have been reported. Here, we found an increased HIV-inhibitory activity of monoclonal IgG and purified polyclonal IgG when immature monocyte-derived dendritic cells (iMDDCs) were used as target cells instead of autologous blood lymphocytes. We showed that FcγRII is involved in the mechanism for inhibiting HIV-1 infection of iMDDCs by IgG, whereas no induction of maturation was detected at concentrations of IgG that result in a 90% reduction of HIV replication. After induction of FcγRI expression on iMDDCs by IFN-γ, an augmentation of the HIV-inhibitory activity of IgG, related to the expression of FcγRI, was observed. Taken together, our results demonstrate the participation of FcγRs in HIV-1 inhibition by IgG when iMDDCs are the targets. We propose that IgG is able to efficiently inhibit HIV-1 replication in iMDDCs and should be one of the components to be induced by vaccination.