A fatal attraction: Mycobacterium tuberculosis and HIV-1 target DC-SIGN to escape immune surveillance

Research output: Contribution to journalReview articleAcademicpeer-review

Abstract

Dendritic cells (DCs) are vital in the defense against pathogens. However, it is becoming increasingly clear that some pathogens subvert DC functions to escape immune surveillance. For example, HIV-1 targets the DC-specific C-type lectin DC-SIGN (DC-specific intercellular-adhesion-molecule-3-grabbing nonintegrin) to hijack DCs for viral dissemination. Binding to DC-SIGN protects HIV-1 from antigen processing and facilitates its transport to lymphoid tissues, where DC-SIGN promotes HIV-1 infection of T cells. Recent studies demonstrate that DC-SIGN is a universal pathogen receptor that also recognizes Ebola, cytomegalovirus and mycobacteria. Mycobacterium tuberculosis targets DC-SIGN by a mechanism that is distinct from that of HIV-1, leading to inhibition of the immunostimulatory function of DC and, hence, promotion of pathogen survival. A better understanding of DC-SIGN-pathogen interactions and their effects on DC function should help to combat infections.

Original languageEnglish
Pages (from-to)153-9
Number of pages7
JournalTrends in Molecular Medicine
Volume9
Issue number4
Publication statusPublished - Apr 2003

Cite this

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title = "A fatal attraction: Mycobacterium tuberculosis and HIV-1 target DC-SIGN to escape immune surveillance",
abstract = "Dendritic cells (DCs) are vital in the defense against pathogens. However, it is becoming increasingly clear that some pathogens subvert DC functions to escape immune surveillance. For example, HIV-1 targets the DC-specific C-type lectin DC-SIGN (DC-specific intercellular-adhesion-molecule-3-grabbing nonintegrin) to hijack DCs for viral dissemination. Binding to DC-SIGN protects HIV-1 from antigen processing and facilitates its transport to lymphoid tissues, where DC-SIGN promotes HIV-1 infection of T cells. Recent studies demonstrate that DC-SIGN is a universal pathogen receptor that also recognizes Ebola, cytomegalovirus and mycobacteria. Mycobacterium tuberculosis targets DC-SIGN by a mechanism that is distinct from that of HIV-1, leading to inhibition of the immunostimulatory function of DC and, hence, promotion of pathogen survival. A better understanding of DC-SIGN-pathogen interactions and their effects on DC function should help to combat infections.",
keywords = "Cell Adhesion Molecules/immunology, Dendritic Cells/immunology, HIV-1/immunology, Humans, Immunologic Surveillance, Lectins, C-Type/immunology, Mannose/metabolism, Mycobacterium tuberculosis/immunology, Receptors, Cell Surface/immunology, T-Lymphocytes/immunology",
author = "{van Kooyk}, Yvette and Ben Appelmelk and Geijtenbeek, {Teunis B H}",
year = "2003",
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journal = "Trends in Molecular Medicine",
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A fatal attraction : Mycobacterium tuberculosis and HIV-1 target DC-SIGN to escape immune surveillance. / van Kooyk, Yvette; Appelmelk, Ben; Geijtenbeek, Teunis B H.

In: Trends in Molecular Medicine, Vol. 9, No. 4, 04.2003, p. 153-9.

Research output: Contribution to journalReview articleAcademicpeer-review

TY - JOUR

T1 - A fatal attraction

T2 - Mycobacterium tuberculosis and HIV-1 target DC-SIGN to escape immune surveillance

AU - van Kooyk, Yvette

AU - Appelmelk, Ben

AU - Geijtenbeek, Teunis B H

PY - 2003/4

Y1 - 2003/4

N2 - Dendritic cells (DCs) are vital in the defense against pathogens. However, it is becoming increasingly clear that some pathogens subvert DC functions to escape immune surveillance. For example, HIV-1 targets the DC-specific C-type lectin DC-SIGN (DC-specific intercellular-adhesion-molecule-3-grabbing nonintegrin) to hijack DCs for viral dissemination. Binding to DC-SIGN protects HIV-1 from antigen processing and facilitates its transport to lymphoid tissues, where DC-SIGN promotes HIV-1 infection of T cells. Recent studies demonstrate that DC-SIGN is a universal pathogen receptor that also recognizes Ebola, cytomegalovirus and mycobacteria. Mycobacterium tuberculosis targets DC-SIGN by a mechanism that is distinct from that of HIV-1, leading to inhibition of the immunostimulatory function of DC and, hence, promotion of pathogen survival. A better understanding of DC-SIGN-pathogen interactions and their effects on DC function should help to combat infections.

AB - Dendritic cells (DCs) are vital in the defense against pathogens. However, it is becoming increasingly clear that some pathogens subvert DC functions to escape immune surveillance. For example, HIV-1 targets the DC-specific C-type lectin DC-SIGN (DC-specific intercellular-adhesion-molecule-3-grabbing nonintegrin) to hijack DCs for viral dissemination. Binding to DC-SIGN protects HIV-1 from antigen processing and facilitates its transport to lymphoid tissues, where DC-SIGN promotes HIV-1 infection of T cells. Recent studies demonstrate that DC-SIGN is a universal pathogen receptor that also recognizes Ebola, cytomegalovirus and mycobacteria. Mycobacterium tuberculosis targets DC-SIGN by a mechanism that is distinct from that of HIV-1, leading to inhibition of the immunostimulatory function of DC and, hence, promotion of pathogen survival. A better understanding of DC-SIGN-pathogen interactions and their effects on DC function should help to combat infections.

KW - Cell Adhesion Molecules/immunology

KW - Dendritic Cells/immunology

KW - HIV-1/immunology

KW - Humans

KW - Immunologic Surveillance

KW - Lectins, C-Type/immunology

KW - Mannose/metabolism

KW - Mycobacterium tuberculosis/immunology

KW - Receptors, Cell Surface/immunology

KW - T-Lymphocytes/immunology

M3 - Review article

VL - 9

SP - 153

EP - 159

JO - Trends in Molecular Medicine

JF - Trends in Molecular Medicine

SN - 1471-4914

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ER -