Open AccessDC-SIGN on B Lymphocytes Is Required For Transmission of HIV-1 to T Lymphocytes
Author(s) -
Giovanna Rappocciolo,
Paolo Piazza,
Craig L. Fuller,
Todd A. Reinhart,
Simon C. Watkins,
David Rowe,
Mariel Jais,
Phalguni Gupta,
Charles R. Rinaldo
Publication year - 2006
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.0020070
Subject(s) - dc sign , cd23 , cd40 , cd86 , cd80 , biology , dendritic cell , virology , monoclonal antibody , interleukin 21 , virus , antigen presenting cell , t cell , antibody , in vitro , antigen , immunology , cytotoxic t cell , immune system , immunoglobulin e , biochemistry
Infection of T cells by HIV-1 can occur through binding of virus to dendritic cell (DC)-specific ICAM-3 grabbing nonintegrin (DC-SIGN) on dendritic cells and transfer of virus to CD4 + T cells. Here we show that a subset of B cells in the blood and tonsils of normal donors expressed DC-SIGN, and that this increased after stimulation in vitro with interleukin 4 and CD40 ligand, with enhanced expression of activation and co-stimulatory molecules CD23, CD58, CD80, and CD86, and CD22. The activated B cells captured and internalized X4 and R5 tropic strains of HIV-1, and mediated trans infection of T cells. Pretreatment of the B cells with anti–DC-SIGN monoclonal antibody blocked trans infection of T cells by both strains of HIV-1. These results indicate that DC-SIGN serves as a portal on B cells for HIV-1 infection of T cells in trans . Transmission of HIV-1 from B cells to T cells through this DC-SIGN pathway could be important in the pathogenesis of HIV-1 infection.