Molecular basis of Trypanosoma cruzi and Leishmania interaction with their host(s): exploitation of immune and defense mechanisms by the parasite leading to persistence and chronicity, features reminiscent of immune system evasion strategies in cancer diseases.
A number of features occurring during host-parasite interactions in Chagas disease caused by the protozoan parasite, Trypanosoma cruzi, and Leishmaniasis, caused by a group of kinetoplastid protozoan parasites are reminiscent of those observed in cancer diseases. In fact,although the cancer is not a single disease, and that T.cruzi and Leishmania are sophisticated eukaryotic parasites presenting a high level of genotypic variability the growth of the parasites in their host and that of cancer cells share at least one common feature, that is their mutual capacity for rapid cell division. Surprisingly, the parasitic diseases and cancers share some immune evasion strategies. Consideration of these immunological alterations must be added to the evaluation of the pathogenic processes. The molecular and functional characterization of virulence factors and the study of their effect on the arms of the immune system have greatly improved understanding of the regulation of immune effectors functions. The purpose of this review is to analyze some of the current data related to the regulatory components or processes originating from the parasite that control or interfere with host cell physiology. Attempts are also made to delineate some similarities between the immune evasion strategies that parasites and tumors employ. The elucidation of the mode of action of parasite virulence factors toward the host cell allow not only provide us with a more comprehensive view of the host-parasite relationships but may also represent a step forward in efforts aimed to identify new target molecules for therapeutic intervention.
Ouaissi
Ali
A
IRD, Research Unit No.008, The Pathogenesis of Trypanosomatides, Centre IRD de Montpellier, Montpellier, France. ali.ouaissi@montp.inserm.fr
Ouaissi
Mehdi
M
D000818:Animals; D000953:Antigens, Protozoan; D017209:Apoptosis; D014355:Chagas Disease / Q000276:immunology / Q000469:parasitology; D003165:Complement System Proteins / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D006790:Host-Parasite Interactions / Q000276:immunology*; D006801:Humans; D007891:Leishmania / Q000276:immunology* / Q000472:pathogenicity*; D007896:Leishmaniasis / Q000276:immunology / Q000469:parasitology; D008213:Lymphocyte Activation; D018448:Models, Immunological; D009369:Neoplasms / Q000276:immunology*; D009569:Nitric Oxide / Q000096:biosynthesis; D014349:Trypanosoma cruzi / Q000276:immunology* / Q000472:pathogenicity*
D000953:Antigens, Protozoan; D016207:Cytokines; D009569:Nitric Oxide; D003165:Complement System Proteins