DC-SIGN, a Dendritic Cell–Specific HIV-1-Binding Protein that Enhances trans-Infection of T Cells

  title={DC-SIGN, a Dendritic Cell–Specific HIV-1-Binding Protein that Enhances trans-Infection of T Cells},
  author={Teunis B. H. Geijtenbeek and Douglas S. Kwon and Ruurd Torensma and Sandra J. van Vliet and Gerard C.F van Duijnhoven and Jeena Middel and Ine M. H. A. Cornelissen and Hans S. L. M. Nottet and Vineet N. KewalRamani and Dan R. Littman and Carl G. Figdor and Yvette van Kooyk},

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DC-SIGN, a dentritic cell-specific HIV-1 receptor present in placenta that infects T cells in trans-a review.

A DC-specific C-type lectin that is highly expressed on DC present in mucosal tissues and binds to the HIV-1 envelope glycoprotein gp120 is described that promotes efficient infection in trans of cells that express CD4 and chemokine receptors.

DC-SIGN promotes exogenous MHC-I-restricted HIV-1 antigen presentation.

It is shown that DC-SIGN expression in B-cell lines dramatically enhances viral internalization and the lectin does not significantly protect captured virions against degradation and promotes MHC-I exogenous presentation of HIV-1 antigens.

Dendritic Cell-Mediated trans-Enhancement of Human Immunodeficiency Virus Type 1 Infectivity Is Independent of DC-SIGN

Dendritic cells enhance human immunodeficiency virus type 1 (HIV-1) infection of CD4+ T lymphocytes in trans using a short hairpin RNA approach, demonstrating that DC-SIGN is not required for efficient trans-enhancement by DCs.

Cell type-dependent retention and transmission of HIV-1 by DC-SIGN.

The function of DC-SIGN in HIV-1 transmission depends on its cellular context, since only DC and the THP monocyte cell line, but not 293 and HOS, are able to useDC-SIGN to retain HIV- 1 in a highly infectious state for several days.

DC-SIGN on B Lymphocytes Is Required For Transmission of HIV-1 to T Lymphocytes

It is shown 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, andCD22.

NOTES Dendritic Cell-Mediated trans -Enhancement of Human Immunodeficiency Virus Type 1 Infectivity Is Independent of DC-SIGN (cid:1)

Using a short hairpin RNA approach, it is demonstrated that DC-SIGN is not required for DC-mediated trans-enhancement of HIV infectivity and HIV-1 particles were internalized and were protected from protease treatment following binding to DCs.

Presentation to T Cells Receptor DC-SIGN Internalizes Antigen for The Dendritic Cell-Specific Adhesion

It is demonstrated that on DCs DC-SIGN is rapidly internalized upon binding of soluble ligand, and detailed analysis using ratio fluorescence imaging and electron microscopy showed thatDC-SIGN-ligand complexes are targeted to late endosomes/lysosomes.

DC-SIGN Increases the Affinity of HIV-1 Envelope Glycoprotein Interaction with CD4

DC-SIGN binding to the HIV envelope protein effectively increases exposure of the CD4 binding site, which in turn contributes to enhancement of infection.



A dendritic-cell-derived C–C chemokine that preferentially attracts naive T cells

The specific expression of DC-CK1 by dendritic cells at the site of initiation of an immune response, combined with its chemotactic activity for naive T cells, suggests that DC- cK1 has an important rule in the induction of immune responses.

Productive infection of dendritic cells by HIV-1 and their ability to capture virus are mediated through separate pathways.

It is suggested that strategies designed to block mucosal transmission of HIV should consider interfering with both virus infection and virus capture by DC.

Efficient Interaction of HIV-1 with Purified Dendritic Cells via Multiple Chemokine Coreceptors

While HIV-1 does not replicate efficiently in mature DCs, viral entry can be active and can be blocked by chemokines that act on known receptors for M- and T-tropic virus.

Dendritic cells exposed to human immunodeficiency virus type-1 transmit a vigorous cytopathic infection to CD4+ T cells.

Carriage of HIV-1 by dendritic cells may facilitate the lysis and loss of antigen specific CD4+ T cells in acquired immunodeficiency syndrome.

Dendritic Cell–T-Cell Interactions Support Coreceptor-Independent Human Immunodeficiency Virus Type 1 Transmission in the Human Genital Tract

It is indicated that HIV-1 can exploit T-cell–DC synergism in the human genital tract to overcome potential coreceptor restrictions on DC and postentry blocks of viral replication in unactivated T cells.

HIV-1 entry into CD4+ cells is mediated by the chemokine receptor CC-CKR-5

The β-chemokines MIP-1α, MIP-1β and RANTES inhibit infection of CD4+ cells by primary, non-syncytium-inducing (NSI) HIV-1 strains at the virus entry stage, and also block env-mediated cell–cell

Dendritic cells and the replication of HIV‐1

The literature leads to the hypothesis that HIV‐1 infection is a battleground in which DCs could be leading both of the armies, the aggressor that promotes HIV‐ 1 replication from relatively small numbers of infected cells and the defender that mediates T cell‐dependent resistance.

Human immunodeficiency virus-1 entry into purified blood dendritic cells through CC and CXC chemokine coreceptors.

The coexpression of multiple chemokine receptors offers a molecular mechanism to explain the permissiveness of DC for both M- and T-tropic viruses.