CD8+ T cells and IFN-γ mediate the time-dependent accumulation of infected red blood cells in deep organs during experimental cerebral malaria. - Test2 - elhamkhani - TriplyDB

CD8+ T cells and IFN-γ mediate the time-dependent accumulation of infected red blood cells in deep organs during experimental cerebral malaria.

CD8+ T cells and IFN-γ mediate the time-dependent accumulation of infected red blood cells in deep organs during experimental cerebral malaria.

http://www.wikidata.org/entity/Q33873437

about

Cerebral malaria: mysteries at the blood-brain barrier Cerebral malaria: gamma-interferon redux Does EBV alter the pathogenesis of malaria?The Combined Deficiency of Immunoproteasome Subunits Affects Both the Magnitude and Quality of Pathogen- and Genetic Vaccination-Induced CD8+ T Cell Responses to the Human Protozoan Parasite Trypanosoma cruzi Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier Real-time imaging reveals the dynamics of leukocyte behaviour during experimental cerebral malaria pathogenesis Nitric oxide synthase dysfunction contributes to impaired cerebroarteriolar reactivity in experimental cerebral malaria Neuroimmunological blood brain barrier opening in experimental cerebral malaria Absence of apolipoprotein E protects mice from cerebral malaria Enlightening the malaria parasite life cycle: bioluminescent Plasmodium in fundamental and applied research Glucocorticosteroids in nano-sterically stabilized liposomes are efficacious for elimination of the acute symptoms of experimental cerebral malaria Toxoplasma gondii upregulates interleukin-12 to prevent Plasmodium berghei-induced experimental cerebral malaria.Increased survival in B-cell-deficient mice during experimental cerebral malaria suggests a role for circulating immune complexes.Imaging Plasmodium immunobiology in the liver, brain, and lung.Effect of mature blood-stage Plasmodium parasite sequestration on pathogen biomass in mathematical and in vivo models of malaria.Simultaneously targeting inflammatory response and parasite sequestration in brain to treat Experimental Cerebral Malaria Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.Reduction of experimental cerebral malaria and its related proinflammatory responses by the novel liposome-based β-methasone nanodrug.Interferons and interferon regulatory factors in malaria Protection from experimental cerebral malaria with a single dose of radiation-attenuated, blood-stage Plasmodium berghei parasites.Role of the aryl hydrocarbon receptor in the immune response profile and development of pathology during Plasmodium berghei Anka infection Inflammatory Flt3l is essential to mobilize dendritic cells and for T cell responses during Plasmodium infection.Sequestration and histopathology in Plasmodium chabaudi malaria are influenced by the immune response in an organ-specific manner Inflammatory responses associated with the induction of cerebral malaria: lessons from experimental murine models Damage to the blood-brain barrier during experimental cerebral malaria results from synergistic effects of CD8+ T cells with different specificities Lipoxin A₄ and 15-epi-lipoxin A₄ protect against experimental cerebral malaria by inhibiting IL-12/IFN-γ in the brain Angiotensin II is a new component involved in splenic T lymphocyte responses during Plasmodium berghei ANKA infection.Irf8-regulated genomic responses drive pathological inflammation during cerebral malaria.Endothelial cells potentiate interferon-γ production in a novel tripartite culture model of human cerebral malaria.Dietary restriction protects against experimental cerebral malaria via leptin modulation and T-cell mTORC1 suppression Malaria induces anemia through CD8+ T cell-dependent parasite clearance and erythrocyte removal in the spleen.Iron prevents the development of experimental cerebral malaria by attenuating CXCR3-mediated T cell chemotaxis.Phosphatidylinositol 3-Kinase γ is required for the development of experimental cerebral malaria.Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.Activated Brain Endothelial Cells Cross-Present Malaria Antigen The CTLA-4 and PD-1/PD-L1 inhibitory pathways independently regulate host resistance to Plasmodium-induced acute immune pathology.Disruption of Parasite hmgb2 Gene Attenuates Plasmodium berghei ANKA Pathogenicity.Platelets present antigen in the context of MHC class I.IFN-γ-producing CD4+ T cells promote experimental cerebral malaria by modulating CD8+ T cell accumulation within the brain.

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CD8+ T cells and IFN-γ mediate the time-dependent accumulation of infected red blood cells in deep organs during experimental cerebral malaria.

http://www.wikidata.org/entity/Q33873437

description

2011 nî lūn-bûn

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2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria.

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria.

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria.

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria.

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria.

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CD8+ T cells and IFN-γ mediate ...... experimental cerebral malaria

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Alicia Yoke Wei Wong

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Florent Ginhoux

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Laurent Rénia

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Zi Wei Chang

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P2860

Estimating the global clinical burden of Plasmodium falciparum malaria in 2007

Molecular aspects of severe malaria

Shrinking the malaria map: progress and prospects

Estimation of the total parasite biomass in acute falciparum malaria from plasma PfHRP2

Both functional LTbeta receptor and TNF receptor 2 are required for the development of experimental cerebral malaria

Sequestration and Tissue Accumulation of Human Malaria Parasites: Can We Learn Anything from Rodent Models of Malaria?

Severe falciparum malaria. World Health Organization, Communicable Diseases Cluster

The pathogenic basis of malaria

Murine malaria parasite sequestration: CD36 is the major receptor, but cerebral pathology is unlinked to sequestration.

A role for natural regulatory T cells in the pathogenesis of experimental cerebral malaria.

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4

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6

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Benoit Malleret

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51052686

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cerebral malaria

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3073989

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