Leishmaniasis: complexity at the host–pathogen interface View Full Text


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Article Info

DATE

2011-07-11

AUTHORS

Paul Kaye, Phillip Scott

ABSTRACT

Key PointsMany Leishmania spp. can cause human disease, with clinical symptoms dependent upon both host- and parasite-related factors.During infection, leishmanial parasites may be phagocytosed by a variety of cells, including neutrophils, monocytes, monocyte-derived dendritic cells (moDCs), macrophages and stromal cells. However, host cell preference and the importance of each cell type to parasite clearance versus parasite persistence may vary following infection by different Leishmania spp.Intracellular Leishmania parasites have multiple ways to manipulate macrophage function, including subverting the control of phagosome biogenesis and maturation. The importance of parasite virulence factors (for example, lipophosphoglycan) in this process is dependent upon leishmanial species and host cell type.Major surface protease (MSP; also known as GP63) of Leishmania spp. has an important role in regulating intracellular survival in some host cells, by cleaving a variety of phosphotyrosine phosphatases such as SRC homology 2 domain phosphotyrosine receptor phosphate (SHP1). MSP may access these cytosolic targets after crossing lipid microdomains in the host cell membrane.Iron has a key role in intracellular survival of leishmanial pathogens, with both host (SLC11A1) and parasite (LIT1) transporters competing to secure this essential resource.Cell-mediated immunity to leishmanial infection is multifactorial, with different models of disease serving to exemplify different aspects, for example, the importance of CD8+ T cells and/or the involvement of moDCs.Parasite persistence and the capacity to induce good vaccine-induced immunity are both strongly influenced by the presence of interleukin-10 (IL-10). There are multiple cellular sources of IL-10 (T helper 1 (TH1) cells, regulatory T (TReg) cells, B cells, macrophages and DCs), but whether each has similar functional significance has yet to be determined. More... »

PAGES

604-615

References to SciGraph publications

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  • 2002-12. CD4+CD25+ regulatory T cells control Leishmania major persistence and immunity in NATURE
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  • 2009-02-08. Cholesterol depletion associated with Leishmania major infection alters macrophage CD40 signalosome composition and effector function in NATURE IMMUNOLOGY
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  • 2007-12. Macrophage tolerance: CD47–SIRP-α–mediated signals matter in NATURE IMMUNOLOGY
  • 2006-05-12. The SIRP family of receptors and immune regulation in NATURE REVIEWS IMMUNOLOGY
  • 2009-03-20. Transcriptional signatures of BALB/c mouse macrophages housing multiplying Leishmania amazonensis amastigotes in BMC GENOMICS
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    http://scigraph.springernature.com/pub.10.1038/nrmicro2608

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/21747391


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