Different Epitopes of the Macrophage Type Three Complement Receptor (CR3) Are Used to Bind Leishmania Promastigotes Harvested at Different Phases of Their Growth Cycle

Cooper, Andrea; Wozencraft, A O; Roach, T. I. A.; Blackwell, Jenefer M.

doi:10.1007/978-1-4613-1575-9_34

Cited by 17 publications

(20 citation statements)

References 18 publications

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“…Following infection, footpad inflammation was monitored as an indicator of disease progression (9,18). As expected, C57BL/6 mice displayed an initial period of footpad swelling lasting ϳ35 days, but thereafter the swelling decreased to near normal by 91 days (Fig.…”

Section: Overexpression Of Il-13 Promotes Susceptibility In Otherwisementioning

confidence: 65%

“…major (LV39) was maintained as described (18). Soluble Leishmania Ag (SLA) 3 was prepared by rapidly freeze thawing a pellet of 5.6 ϫ 10 9 L. major promastigotes.…”

Section: Parasites and Leishmania Agmentioning

confidence: 99%

“…IL-13-Tg (15) and control C57BL/6 mice were infected in the rear footpad with L. major LV39 promastigotes (9,18). Following infection, footpad inflammation was monitored as an indicator of disease progression (9,18).…”

Section: Overexpression Of Il-13 Promotes Susceptibility In Otherwisementioning

confidence: 99%

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IL-13 Is a Susceptibility Factor forLeishmania majorInfection

Matthews

Emson

McKenzie

et al. 2000

The Journal of Immunology

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140

109

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Leishmania major infection is useful as an experimental model to define factors responsible for the development and maintenance of Th cell immune responses. Studies using inbred mouse strains have identified that the Th1 response characteristic of C57BL/6 mice results in healing, whereas BALB/c mice fail to control the infection due to the generation of an inappropriate Th2 response. We now demonstrate that IL-13 is a key factor in determining susceptibility to L. major infection. Overexpression of IL-13 in transgenic mice makes the normally resistant C57BL/6 mouse strain susceptible to L. major infection even in the absence of IL-4 expression. This susceptibility correlates with a suppression of IL-12 and IFN-γ expression. Furthermore, using BALB/c mice deficient in the expression of IL-4, IL-13, or both IL-13 and IL-4, we demonstrate that IL-13-deficient mice are resistant to infection and that there is an additive effect of deleting both IL-4 and IL-13.

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Section: Overexpression Of Il-13 Promotes Susceptibility In Otherwisementioning

confidence: 65%

“…major (LV39) was maintained as described (18). Soluble Leishmania Ag (SLA) 3 was prepared by rapidly freeze thawing a pellet of 5.6 ϫ 10 9 L. major promastigotes.…”

Section: Parasites and Leishmania Agmentioning

confidence: 99%

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IL-13 Is a Susceptibility Factor forLeishmania majorInfection

Matthews

Emson

McKenzie

et al. 2000

The Journal of Immunology

Self Cite

140

109

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“…1D) in the presence of anti-CR3 mAbs M1/70 and 5C6 (Cooper et al, 1988;Rosen and Gordon, 1987;Xia et al, 1999). The two mAbs bind to distinct epitopes in CR3 a M subunit: M1/70 to a C3bi site and 5C6 to a lectin, b-glucan site.…”

Section: Cr3 In Cns Microglia Mediates the Phagocytosis Of C3bi-opsonmentioning

confidence: 91%

Dissimilar and similar functional properties of complement receptor‐3 in microglia and macrophages in combating yeast pathogens by phagocytosis

Hadas¹,

Reichert²,

Rotshenker³

2010

Glia

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Central nervous system (CNS) microglia (MG) and peripheral tissue macrophages (MO) remove pathogens by phagocytosis. Zymosan, a model yeast pathogen, is a beta-glucan rich particle that readily activates the complement system and then becomes C3bi-opsonized (op). Complement receptor-3 (CR3) has initially been implicated in mediating the phagocytosis of both C3bi-op and non-opsonized (nop) zymosan by MO through C3bi and beta-glucan binding sites, respectively. Later, the role of CR3 as a phagocytic beta-glucan receptor has been questioned and the supremacy of beta-glucan receptor Dectin-1 advocated. We compare here between primary mouse CNS MG and peripheral tissue MO with respect to CR3 and Dectin-1 mediated phagocytosis of C3bi-op and nop zymosan. We report that MG and MO display similar as well as dissimilar functional properties in this respect. Although CR3 and Dectin-1 function both as beta-glucan/non-opsonic receptors in MG during nop zymosan phagocytosis, Dectin-1, but not CR3, does so in MO. CR3 functions also as a C3bi/opsonic receptor in MG and MO during C3bi-op zymosan phagocytosis, leading to phagocytosis which is more efficient than that of nop zymosan. Dectin-1 contributes, albeit less than CR3, to phagocytosis of C3bi-op zymosan in MG and further less in MO, suggesting that C3bi-opsonization does not block all beta-glucan sites on zymosan from binding Dectin-1 on phagocytes. Thus, altogether CR3 and Dectin-1 contribute both to phagocytosis of nop and C3bi-op zymosan in MG, whereas MO switch from CR3-independent/Dectin-1-dependent phagocytosis of nop zymosan to phagocytosis of C3bi-op zymosan where CR3 dominates over Dectin-1.

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“…369 Opsonization with these complement components mediates promastigote uptake by binding to the macrophage complement receptors CR1 and CR3, respectively. 40, 370,371,372,373,374,375,376,377 The parasite surface molecule gp63 contains a Ser-Arg-Tyr-Asp sequence that mimics the cell attachment sequence of Arg-Gly-AspSer (RGDS) of fibronectin, and as such Leishmania spp. use the RGDS binding domains of the fibronectin receptor for attachment to macrophages.…”

Section: B Receptor-mediated Entry Of Leishmania Into Host Macrophagesmentioning

confidence: 99%

Macrophage-Mediated Innate Host Defense Against Protozoan Parasites

Stafford

Neumann

Belosevic

2002

Critical Reviews in Microbiology

127

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Macrophages are immune cells that play a pivotal role in the detection and elimination of pathogenic microorganisms. Macrophages possess a variety of surface receptors devoted to the recognition of non-self by discriminating between host and pathogen-derived structures. Recognition of foreign microorganisms by the macrophage ultimately results in phagocytosis and the eventual destruction of microorganisms by lysosomal enzymes, toxic reactive oxygen and nitrogen intermediates, and/or nutrient deprivational mechanisms. However, protozoan parasites such as Toxoplasma gondii, Trypanosoma cruzi, and Leishmania spp., parasitize macrophages, utilizing them as a host cell for their growth, replication, and/or maintenance of their life cycles. The protozoan parasites of the genus Leishmania are unique in that their intracellular replication in the host is predominantly restricted to a single cell type, the macrophage. This review focuses on the cellular processes involved in macrophage-mediated host defense against protozoan parasites, from the initial host-parasite interactions that mediate recognition to the mechanisms employed by macrophages to destroy and eliminate the pathogen. As an example model system of experimental study, we describe in more more detail the cellular interactions between macrophages and the obligate intracellular parasite of mammalian macrophages, Leishmania spp.

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Different Epitopes of the Macrophage Type Three Complement Receptor (CR3) Are Used to Bind Leishmania Promastigotes Harvested at Different Phases of Their Growth Cycle

Cited by 17 publications

References 18 publications

IL-13 Is a Susceptibility Factor forLeishmania majorInfection

IL-13 Is a Susceptibility Factor forLeishmania majorInfection

Dissimilar and similar functional properties of complement receptor‐3 in microglia and macrophages in combating yeast pathogens by phagocytosis

Macrophage-Mediated Innate Host Defense Against Protozoan Parasites

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