Dendritic cells and parasites: from recognition and activation to immune response instruction

Semin Immunopathol. 2017 Feb;39(2):199-213. doi: 10.1007/s00281-016-0588-7. Epub 2016 Sep 1.


The effective defense against parasite infections requires the ability to mount an appropriate and controlled specific immune response able to eradicate the invading pathogen while limiting the collateral damage to self-tissues. Dendritic cells are key elements for the development of immunity against parasites; they control the responses required to eliminate these pathogens while maintaining host homeostasis. Ligation of dendritic cell pattern recognition receptors by pathogen-associated molecular pattern present in the parasites initiates signaling pathways that lead to the production of surface and secreted proteins that are required, together with the antigen, to induce an appropriate and timely regulated immune response. There is evidence showing that parasites can influence and regulate dendritic cell functions in order to promote a more permissive environment for their survival. In this review, we will focus on new insights about the ability of protozoan and helminth parasites or their products to modify dendritic cell function and discuss how this interaction is crucial in shaping the host response.

Keywords: Helminth; Protozoa; Th cell polarization; Tissue damage; Tolerance.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism*
  • Host-Parasite Interactions / immunology*
  • Humans
  • Immune System / cytology
  • Immune System / immunology
  • Immune System / metabolism
  • Immune Tolerance
  • Janus Kinases / metabolism
  • Parasites / immunology*
  • Parasitic Diseases / immunology*
  • Parasitic Diseases / metabolism*
  • Parasitic Diseases / parasitology
  • STAT Transcription Factors / metabolism
  • Signal Transduction
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • Toll-Like Receptors / metabolism


  • STAT Transcription Factors
  • Toll-Like Receptors
  • Janus Kinases