Subversion of host cell signalling by the protozoan parasite Leishmania

D J Gregory1, M Olivier

  • 1Centre for the Study of Host Resistance, Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.

Parasitology
|November 12, 2005
PubMed

Insights

Leishmania parasites evade host immunity by manipulating macrophage signaling pathways. This review details how Leishmania species suppress key macrophage functions, including cytokine production and antigen presentation.

Area of Science:

  • Immunology
  • Parasitology
  • Cell Biology

Background:

  • Leishmania spp. are obligate intracellular protozoan parasites residing within host macrophages.
  • Macrophages are crucial immune cells responsible for pathogen destruction and initiating immune responses.
  • Leishmania have developed sophisticated mechanisms to evade macrophage-mediated killing and immune surveillance.

Purpose of the Study:

  • To review the intricate strategies employed by Leishmania to subvert host macrophage functions.
  • To elucidate the molecular mechanisms through which Leishmania disrupts macrophage signaling pathways.
  • To highlight the impact of Leishmania infection on cytokine expression, microbicidal activity, and antigen presentation.

Main Methods:

  • This review synthesizes existing research on Leishmania-macrophage interactions.
  • It analyzes the manipulation of host cell signaling cascades, including MAP Kinase and JAK/STAT pathways.
  • Focus is placed on alterations in intracellular calcium levels and protein tyrosine phosphatase activity.

Main Results:

  • Leishmania actively suppresses the expression of critical cytokines and microbicidal molecules (nitric oxide, reactive oxygen species).
  • The parasites interfere with antigen presentation capabilities of macrophages.
  • Key signaling pathways such as MAP Kinase and JAK/STAT are demonstrably repressed.

Conclusions:

  • Leishmania effectively manipulates host macrophage signaling to promote its survival and replication.
  • Understanding these evasion strategies is crucial for developing effective anti-Leishmania therapies.
  • Targeting host-pathogen signaling crosstalk offers potential therapeutic avenues.

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