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  • 1
    Online Resource
    Online Resource
    Placental Malaria-Associated Suppression of Parasite-Specific Immune Response in Neonates Has No Major Impact on Systemic CD4 T Cell Homeostasis
    American Society for Microbiology ; 2011
    In:  Infection and Immunity Vol. 79, No. 7 ( 2011-07), p. 2801-2809
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 79, No. 7 ( 2011-07), p. 2801-2809
    Abstract: In areas where Plasmodium falciparum is endemic, pregnancy is associated with accumulation of infected red blood cells (RBCs) in the placenta, a condition referred to as placental malaria (PM). Infants born to PM-positive mothers are at an increased risk of malaria, which is putatively related to the transplacental passage of parasite-derived antigens, with consequent tolerization of the fetal immune system. Here we addressed the impact of PM on the regulation of neonatal T cell responses. We found that the frequency of regulatory CD25 + CD127 −/low Foxp3 + CD4 + T cells was significantly decreased in neonates born to mothers with high levels of P. falciparum -induced placental inflammation, consisting mainly of primigravid mothers. However, at the individual level, the ratio between regulatory and effector (CD25 + CD127 + Foxp3 − ) CD4 + T cells was unaffected by PM. In addition, parasite-induced CD4 + T cell activation and production of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and IL-10 were strongly reduced in neonates born to PM-positive mothers. Thus, our results show that active PM at delivery is associated with a marked suppression of P. falciparum -specific cellular neonatal immune responses, affecting secretion of both pro- and anti-inflammatory cytokines. Additionally, our results suggest that, as in adults, effector and regulatory CD4 + T cell populations are tightly coregulated in all neonates, irrespective of the maternal infection status.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00203-11
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2011
    detail.hit.zdb_id: 1483247-1
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  • 2
    Online Resource
    Online Resource
    Primary Infection of C57BL/6 Mice with Plasmodium yoelii Induces a Heterogeneous Response of NKT Cells
    American Society for Microbiology ; 2007
    In:  Infection and Immunity Vol. 75, No. 5 ( 2007-05), p. 2511-2522
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 75, No. 5 ( 2007-05), p. 2511-2522
    Abstract: NKT cells are a population of innate-like lymphocytes that display effector functions and immunoregulatory properties. We characterized the NKT cell response induced in C57BL/6 mice during a primary infection with Plasmodium yoelii sporozoites. We observed a heterogeneous NKT cell response that differed between liver and spleen. Hepatic NKT cells found in infected livers consisted mainly of CD1d-dependent CD4 + and double-negative (DN) NKT cells, whereas CD1d-independent NKT cells exhibiting a TCR high CD4 high phenotype were prominent among splenic NKT cells during the infection. Hepatic and splenic NKT cells isolated from infected mice were activated and secreted mainly gamma interferon and tumor necrosis factor alpha in response to stimulation. Finally, P. yoelii -activated hepatic DN NKT cells inhibited the parasite's liver stage in a CD1d-dependent manner in vitro. However, experiments using B6.CD1d-deficient mice showed that CD1d and CD1d-restricted NKT cells are not necessary to control the parasite's development in vivo during neither the preerythrocytic stage nor the erythrocytic stage. Thus, our results show that a primary P. yoelii infection induces a heterogeneous and organ-specific response of NKT cells and that CD1d-dependent NKT cells play a minor role in the control of the development of Plasmodium in vivo in our model.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.01818-06
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
    detail.hit.zdb_id: 1483247-1
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  • 3
    Online Resource
    Online Resource
    Chloroquine Potentiates Primaquine Activity against Active and Latent Hepatic Plasmodia Ex Vivo : Potentials and Pitfalls
    American Society for Microbiology ; 2020
    In:  Antimicrobial Agents and Chemotherapy Vol. 65, No. 1 ( 2020-12-16)
    Details
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 65, No. 1 ( 2020-12-16)
    Abstract: For a long while, 8-aminoquinoline compounds have been the only therapeutic agents against latent hepatic malaria parasites. These have poor activity against the blood-stage plasmodia causing acute malaria and must be used in conjunction with partner blood schizontocidal agents. We examined the impacts of one such agent, chloroquine, upon the activity of primaquine, an 8-aminoquinoline, against hepatic stages of Plasmodium cynomolgi , Plasmodium yoelii , Plasmodium berghei , and Plasmodium falciparum within several ex vivo systems—primary hepatocytes of Macaca fascicularis , primary human hepatocytes, and stably transformed human hepatocarcinoma cell line HepG2. Primaquine exposures to formed hepatic schizonts and hypnozoites of P. cynomolgi in primary simian hepatocytes exhibited similar 50% inhibitory concentration (IC 50 ) values near 0.4 μM, whereas chloroquine in the same system exhibited no inhibitory activities. Combining chloroquine and primaquine in this system decreased the observed primaquine IC 50 for all parasite forms in a chloroquine dose-dependent manner by an average of 18-fold. Chloroquine also decreased the primaquine IC 50 against hepatic P. falciparum in primary human hepatocytes, P. berghei in simian primary hepatocytes, and P. yoelii in primary human hepatocytes. Chloroquine had no impact on primaquine IC 50 against P. yoelii in HepG2 cells and, likewise, had no impact on the IC 50 of atovaquone (hepatic schizontocide) against P. falciparum in human hepatocytes. We describe important sources of variability in the potentiation of primaquine activity by chloroquine in these systems. Chloroquine potentiated primaquine activity against hepatic forms of several plasmodia. We conclude that chloroquine specifically potentiated 8-aminoquinoline activities against active and dormant hepatic-stage plasmodia in normal primary hepatocytes but not in a hepatocarcinoma cell line.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    URL: Article
    DOI: 10.1128/AAC.01416-20
    RVK:
    XA 24552
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2020
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    NK Cell Responses to Plasmodium Infection and Control of Intrahepatic Parasite Development
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 177, No. 2 ( 2006-07-15), p. 1229-1239
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 177, No. 2 ( 2006-07-15), p. 1229-1239
    Abstract: Various components of innate and adaptive immunity contribute to host defenses against Plasmodium infection. We investigated the contribution of NK cells to the immune response to primary infection with Plasmodium yoelii sporozoites in C57BL/6 mice. We found that hepatic and splenic NK cells were activated during infection and displayed different phenotypic and functional properties. The number of hepatic NK cells increased whereas the number of splenic NK cells decreased. Expression of the Ly49 repertoire was modified in the spleen but not in the liver. Splenic and hepatic NK cells have a different inflammatory cytokines profile production. In addition, liver NK cells were cytotoxic to YAC-1 cells and P. yoelii liver stages in vitro but not to erythrocytic stages. No such activity was observed with splenic NK cells from infected mice. These in vitro results were confirmed by the in vivo observation that Rag2−/− mice were more resistant to sporozoite infection than Rag2−/− γ c−/− mice, whereas survival rates were similar for the two strains following blood-stage infection. Thus, NK cells are involved in early immune mechanisms controlling Plasmodium infection, mostly at the pre-erythrocytic stage.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.177.2.1229
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Liver CD4−CD8− NK1.1+ TCRαβ Intermediate Cells Increase During Experimental Malaria Infection and Are Able to Exhibit Inhibitory Activity Against the Parasite Liver Stage In Vitro
    The American Association of Immunologists ; 2000
    In:  The Journal of Immunology Vol. 164, No. 3 ( 2000-02-01), p. 1463-1469
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 164, No. 3 ( 2000-02-01), p. 1463-1469
    Abstract: Experimental infection of C57BL/6 mice by Plasmodium yoelii sporozoites induced an increase of CD4−CD8− NK1.1+ TCRαβint cells and a down-regulation of CD4+ NK1.1+ TCRαβint cells in the liver during the acute phase of the infection. These cells showed an activated CD69+, CD122+, CD44high, and CD62Lhigh surface phenotype. Analysis of the expressed TCRVβ segment repertoire revealed that most of the expanded CD4−CD8− (double-negative) T cells presented a skewed TCRVβ repertoire and preferentially used Vβ2 and Vβ7 rather than Vβ8. To get an insight into the function of expanded NK1.1+ T cells, experiments were designed in vitro to study their activity against P. yoelii liver stage development. P. yoelii-primed CD3+ NK1.1+ intrahepatic lymphocytes inhibited parasite growth within the hepatocyte. The antiplasmodial effector function of the parasite-induced NK1.1+ liver T cells was almost totally reversed with an anti-CD3 Ab. Moreover, IFN-γ was in part involved in this antiparasite activity. These results suggest that up-regulation of CD4−CD8− NK1.1+ αβ T cells and down-regulation of CD4+ NK1.1+ TCRαβint cells may contribute to the early immune response induced by the Plasmodium during the prime infection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.164.3.1463
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2000
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Cutting Edge: Crucial Role of IL-1 and IL-23 in the Innate IL-17 Response of Peripheral Lymph Node NK1.1− Invariant NKT Cells to Bacteria
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 2 ( 2011-01-15), p. 662-666
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 2 ( 2011-01-15), p. 662-666
    Abstract: We have shown previously that peripheral lymph node-resident retinoic acid receptor-related orphan receptor γt+ NK1.1− invariant NKT (iNKT) cells produce IL-17A independently of IL-6. In this study, we show that the concomitant presence of IL-1 and IL-23 is crucial to induce a rapid and sustained IL-17A/F and IL-22 response by these cells that requires TCR–CD1d interaction and partly relies on IL-23–mediated upregulation of IL-23R and IL-1R1 expression. We further show that IL-1 and IL-23 produced by pathogen-associated molecular pattern-stimulated dendritic cells induce this response from NK1.1− iNKT cells in vitro, involving mainly TLR2/4-signaling pathways. Finally, we found that IL-17A production by these cells occurs very early and transiently in vivo in response to heat-killed bacteria. Overall, our study indicates that peripheral lymph node NK1.1− iNKT cells could be a source of innate Th17-related cytokines during bacterial infections and supports the hypothesis that they are able to provide an efficient first line of defense against bacterial invasion.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1002725
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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