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Review
. 2014 Oct 20:5:480.
doi: 10.3389/fimmu.2014.00480. eCollection 2014.

Deception and manipulation: the arms of leishmania, a successful parasite

Pedro Cecílio  1 , Begoña Pérez-Cabezas  1 , Nuno Santarém  1 , Joana Maciel  1 , Vasco Rodrigues  1 , Anabela Cordeiro da Silva  2
Affiliations
Review

Deception and manipulation: the arms of leishmania, a successful parasite

Pedro Cecílio et al. Front Immunol. .

Abstract

Leishmania spp. are intracellular parasitic protozoa responsible for a group of neglected tropical diseases, endemic in 98 countries around the world, called leishmaniasis. These parasites have a complex digenetic life cycle requiring a susceptible vertebrate host and a permissive insect vector, which allow their transmission. The clinical manifestations associated with leishmaniasis depend on complex interactions between the parasite and the host immune system. Consequently, leishmaniasis can be manifested as a self-healing cutaneous affliction or a visceral pathology, being the last one fatal in 85-90% of untreated cases. As a result of a long host-parasite co-evolutionary process, Leishmania spp. developed different immunomodulatory strategies that are essential for the establishment of infection. Only through deception and manipulation of the immune system, Leishmania spp. can complete its life cycle and survive. The understanding of the mechanisms associated with immune evasion and disease progression is essential for the development of novel therapies and vaccine approaches. Here, we revise how the parasite manipulates cell death and immune responses to survive and thrive in the shadow of the immune system.

Keywords: Leishmania; acquired immunity; apoptosis; immunomodulation; innate immunity.

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Figures

Figure 1
Figure 1
Silent entry of Leishmania into the host cells. Live and dead parasites are engulfed by phagocytes. The recognition of the externalized phosphatidylserine present on the cellular membrane of dead parasites induces TGF-β secretion and TNF-α downregulation (1). Neutrophil apoptosis is delayed by Leishmania (2). Both dendritic cells (3) and macrophages (4) remove neutrophil apoptotic bodies carrying Leishmania promastigotes and secrete TGF-β and IL-10. Macrophages (5) can also phagocyte parasites extruded within other macrophage membrane blebs, which in turn promotes the secretion of IL-10.
Figure 2
Figure 2
Leishmania interferes on MHC II antigen presentation process. Leishmania impairs the antigen presentation process through several mechanisms. The parasite is responsible for the downregulation of MHC II in APC (1), sequestration of antigens from the MHC II pathway (2), limitation of the MHC II-peptide-TCR engagement (3), and down-regulation of co-stimulatory (4), and adhesion molecules (5) on APCs and lymphocytes, respectively.
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