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 language | English |
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Pages (from-to) | 153-159 |
Number of pages | 7 |
Journal | Trends in molecular medicine |
Volume | 9 |
Issue number | 4 |
DOIs | |
Publication status | Published - Apr 2003 |
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