Pathogens target DC-SIGN to influence their fate DC-SIGN functions as a pathogen receptor with broad specificity

APMIS. Jul-Aug 2003;111(7-8):698-714. doi: 10.1034/j.1600-0463.2003.11107803.x.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Adhesion / immunology
  • Cell Adhesion Molecules / immunology*
  • Cytomegalovirus / immunology
  • Dendritic Cells / immunology*
  • Dendritic Cells / virology
  • Ebolavirus / immunology
  • HIV Infections / immunology
  • HIV Infections / virology
  • HIV-1 / immunology
  • Humans
  • Lectins, C-Type / immunology*
  • Models, Molecular
  • Mycobacterium tuberculosis / immunology
  • Receptors, Cell Surface / immunology*
  • Receptors, HIV / immunology

Substances

  • Cell Adhesion Molecules
  • DC-specific ICAM-3 grabbing nonintegrin
  • Lectins, C-Type
  • Receptors, Cell Surface
  • Receptors, HIV