Isolation and characterization of infective and non-infective clones of Leishmania tropica

Handman, Emanuela; Hocking, Robyn E.; Mitchell, Graham F.; Spithill, Terry W.

doi:10.1016/0166-6851(83)90039-7

Cited by 148 publications

(71 citation statements)

References 17 publications

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“…Injections were given to mice on day -21 (20x10* parasites with (O O) or without (A A) C parvum), day -14 (4 K 10'' parasites) and day -7 (40x10* parasites with or without C parvum) with V121 challenge on day 0. A feature of this particular experiment is that, the BALB/c.H-2'' mice showed evidence of lale healing, an unusual occurrence with this mouse strain (12). experimental animals and man (18; 19) with perhaps the most slriking data coming recently from the Wellcome laboratory (1).…”

Section: Discussionmentioning

confidence: 99%

Heterologous protection in murine cutaneous leishmaniasis

Handman

1987

Immunol Cell Biol

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Summary. Mice immunized with a glycolipid aniigen (GL) of Leishmania major plus adjuvant are relatively resistanl to subsequent infection with ihis protozoan parasite. The GL is affinity purified on the monoclonal anlibody WIC-79,3 which is L. major-specific and does not react with L. donovani. When another monoclonal, WIC-108.3, which cross-reacts with several Leishmania species, is used to affinity purify GL from L. donovani, the eluted materiai can partially protect genetically resistant mice against L. major. Thus, GL cross-reactions may in part underlie the known protective effects of crude L. donovani antigens against L. miT/or infection. Experiments with live parasites of the/.. ma/or isolate LRC-L119, that is nonpathogenic in mice, that does not survive long in macrophages in vitro, and that has not been shown to contain any WIC-79.3 reactive GL, indicated that this isolate wilt very effectively protect mice againsi subsequent infection. This raises the possibility that GL is only one of at least two different classes of vaccinating antigen capable of protectively immunizing mice in this cutaneous leishmaniasis model.

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Section: Discussionmentioning

confidence: 99%

Heterologous protection in murine cutaneous leishmaniasis

Handman

1987

Immunol Cell Biol

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“…Promastigotes were maintained in vitro at 261C in the biphasic blood agar culture NNN and used in the stationary phase of growth. 35 Infection with L. major In all, 25-36 female mice at 7-10 weeks of age from each of the following groups were injected intradermally at the base of the tail, 36 with 10 6 L. major V121 promastigotes in the stationary phase of growth-Experiment 1: BALB/c, C.B6-lmr1, C.B6-lmr2, C.B6-lmr3, C.B6-(lmr1, lmr2); Experiment 2: C57BL/6, B6.C-lmr1, B6.C-lmr2; and Experiment 3: C57BL/6, BALB/c, B6.C-(lmr1, lmr2), C.B6-(lmr1, lmr2). The average weekly increase was measured for each mouse by a least-squares regression with intercept zero.…”

Section: Parasitesmentioning

confidence: 99%

Leishmaniasis host response loci (lmr1–3) modify disease severity through a Th1/Th2-independent pathway

et al. 2003

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“…Promastigotes of the L. major strain Friedlin VI (MHOM/IL/80/Friedlin) and the cloned line V121 derived from MHOM/IL/67/Jericho II (WHO Reference Center for Leishmaniasis, Israel) were grown at 26°C in M199 medium with 10% FBS. For infection of mice, promastigotes were grown in the biphasic blood agar medium NNN [39].…”

Section: Cell Lines and Parasitesmentioning

confidence: 99%

MyD88 is essential for clearance of Leishmania major: possible role for lipophosphoglycan and Toll‐like receptor 2 signaling

et al. 2003

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Leishmania major is an obligate intracellular eukaryotic pathogen of mononuclear phagocytes. Invasive promastigotes gain entry into target cells by receptor-mediated phagocytosis, transform into non-motile amastigotes and establish in the phagolysosome. Glycosylphosphatidylinositol-anchored lipophosphoglycan (LPG) is a virulence factor and a major parasite molecule involved in this process. We observed that mice lacking the Toll-like receptor (TLR) pathway adaptor protein MyD88 were more susceptible to infection with L. major than wild-type C57BL/6 mice, demonstrating a central role for this innate immune recognition pathway in control of infection, and suggesting that L. major possesses a ligand for TLR. We sought to identify parasite molecules capable of activating the protective Toll pathway, and found that purified Leishmania LPG, but not other surface glycolipids, activate innate immune signaling pathways via TLR2. Activation of cytokine synthesis by LPG required the presence of the lipid anchor and a functional MyD88 adaptor protein. LPG also induced the expression of negative regulatory pathways mediated by members of the suppressors of cytokine signaling family SOCS-1 and SOCS-3. Thus, the Toll pathway is required for resistance to L. major and LPG is a defined TLR agonist from this important human pathogen.

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Isolation and characterization of infective and non-infective clones of Leishmania tropica

Cited by 148 publications

References 17 publications

Heterologous protection in murine cutaneous leishmaniasis

Heterologous protection in murine cutaneous leishmaniasis

Leishmaniasis host response loci (lmr1–3) modify disease severity through a Th1/Th2-independent pathway

MyD88 is essential for clearance of Leishmania major: possible role for lipophosphoglycan and Toll‐like receptor 2 signaling

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