This review has addressed some of the mechanisms by which Leishmania escapes …

• Summary
• Introduction
• Inhibition of macrophage functions
• Leishmania-induced alteration of host signaling
• Conclusion
• Acknowledgments
• References
• Figures

Biology Articles » Parasitology » Subversion Mechanisms by Which Leishmania Parasites Can Escape the Host Immune Response: a Signaling Point of View » Figures

Figures

- Subversion Mechanisms by Which Leishmania Parasites Can Escape the Host Immune Response: a Signaling Point of View

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FIG. 1. Signaling events leading to the induction or inhibition of macrophage functions during Leishmania infection. Leishmania internalization within the macrophage is a receptor-mediated event, and this initial host-pathogen interaction is responsible for the rapid activation and deactivation of several signaling pathways leading to macrophage functions (e.g., phagocytosis, chemokine secretion, and prostaglandin secretion). SHP-1 negatively affects JAK2, Erk1/Erk2 MAP kinases, NF-B, IRF-1, and AP-1, thus inhibiting IFN--inducible macrophage functions (e.g., nitric oxide, IL-12 production, and immunoproteasome formation). STAT1 degradation by proteasome is PKC dependent. Other phosphatases (e.g., IP₃ phosphatase and calcineurin) and surface parasite molecules (e.g., LPG) play a pivotal role in the alteration of various second messengers (e.g., PKC, Ca²⁺, inositol lipids, and inositol phosphates), regulating important phagocyte functions (e.g., NO and superoxide production). M, macrophage; DAG, diacyl glycerol; PLC, phospholipase C; fMLPR, formyl peptide receptor; PIP2, phosphatidyl inositol 4,5-biphosphate.

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FIG. 2. Activation of SHP-1 in Leishmania-infected macrophages. Naive macrophages or macrophages infected for 30 min with L. donovani were stained with propidium iodide (PI) (red) or antibody specific for SHP-1 (green). SHP-1 is spread evenly throughout the cytoplasm in control cells but adopts a more punctate distribution following infection. Foci of SHP-1 are also visible in the nuclei of infected cells. Nil, no infection; Ld, L. donovani infection.

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Source: Clinical Microbiology Reviews, April 2005, p. 293-305, Vol. 18, No. 2