Abstract
Dendritic cells (DC) are vital in the defense against pathogens. To sense pathogens DC express pathogen recognition receptors such as toll-like receptors (TLR) and C-type lectins that recognize different fragments of pathogens, and subsequently activate or present pathogen fragments to T cells. It is now becoming evident that some pathogens subvert DC functions to escape immune surveillance. HIV-1 targets the DC-specific C-type lectin DC-SIGN to hijack DC for viral dissemination. HIV-1 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 more 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 pathogen survival. Thus, a better understanding of DC-SIGN-pathogen interactions and their effects on DC function is necessary to combat infections.
| Original language | English |
|---|---|
| Pages (from-to) | 698-714 |
| Number of pages | 17 |
| Journal | APMIS. Acta Pathologica, Microbiologica et Immunologica Scandinavica |
| Volume | 111 |
| Issue number | 7-8 |
| DOIs | |
| Publication status | Published - 17 Sept 2003 |
Keywords
- Animals
- Cell Adhesion Molecules/immunology
- Cell Adhesion/immunology
- Cytomegalovirus/immunology
- Dendritic Cells/immunology
- Ebolavirus/immunology
- HIV Infections/immunology
- HIV-1/immunology
- Humans
- Lectins, C-Type/immunology
- Models, Molecular
- Mycobacterium tuberculosis/immunology
- Receptors, Cell Surface/immunology
- Receptors, HIV/immunology