Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria. - Wikidata - wikimedia - TriplyDB

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

http://www.wikidata.org/entity/Q37040808

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Interferon-γ: The Jekyll and Hyde of Malaria Cerebral malaria: gamma-interferon redux 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 Regulation of immunopathogenesis during Plasmodium and Toxoplasma infections: more parallels than distinctions?Splenic differentiation and emergence of CCR5+CXCL9+CXCL10+ monocyte-derived dendritic cells in the brain during cerebral malaria.Plasmodium falciparum histidine-rich protein II causes vascular leakage and exacerbates experimental cerebral malaria in mice.Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.Malaria immunity in man and mosquito: insights into unsolved mysteries of a deadly infectious disease.Interferons and interferon regulatory factors in malaria The subcellular location of ovalbumin in Plasmodium berghei blood stages influences the magnitude of T-cell responses.Damage to the blood-brain barrier during experimental cerebral malaria results from synergistic effects of CD8+ T cells with different specificities Malaria induces anemia through CD8+ T cell-dependent parasite clearance and erythrocyte removal in the spleen.Phosphatidylinositol 3-Kinase γ is required for the development of experimental cerebral malaria.IRGM3 contributes to immunopathology and is required for differentiation of antigen-specific effector CD8+ T cells in experimental cerebral malaria Activated Brain Endothelial Cells Cross-Present Malaria Antigen Inhibiting the Mammalian target of rapamycin blocks the development of experimental cerebral malaria.Targeting glutamine metabolism rescues mice from late-stage cerebral malaria.CD8+ T Cells Induce Fatal Brainstem Pathology during Cerebral Malaria via Luminal Antigen-Specific Engagement of Brain Vasculature.A quantitative brain map of experimental cerebral malaria pathology.Mycobacterium tuberculosis Coinfection Has No Impact on Plasmodium berghei ANKA-Induced Experimental Cerebral Malaria in C57BL/6 Mice.A TCRβ Repertoire Signature Can Predict Experimental Cerebral Malaria.Defining rules of CD8(+) T cell expansion against pre-erythrocytic Plasmodium antigens in sporozoite-immunized mice.Discriminating Protective from Nonprotective Plasmodium-Specific CD8+ T Cell Responses Mice lacking Programmed cell death-1 show a role for CD8(+) T cells in long-term immunity against blood-stage malaria Plasmodium falciparum Histidine-Rich Protein II Compromises Brain Endothelial Barriers and May Promote Cerebral Malaria Pathogenesis.The Deubiquitinating Enzyme Cylindromatosis Dampens CD8+ T Cell Responses and Is a Critical Factor for Experimental Cerebral Malaria and Blood-Brain Barrier Damage Targeting Angiotensin II Type-1 Receptor (AT1R) Inhibits the Harmful Phenotype of Plasmodium-Specific CD8+ T Cells during Blood-Stage Malaria.Host matrix metalloproteinases in cerebral malaria: new kids on the block against blood-brain barrier integrity?Pathogenic CD8+ T cells in experimental cerebral malaria.The immunological balance between host and parasite in malaria.Evidence of cross-stage CD8+ T cell epitopes in malaria pre-erythrocytic and blood stage infections.Investigating proteasome inhibitors as potential adjunct therapies for experimental cerebral malaria.Cross-reactive dengue human monoclonal antibody prevents severe pathologies and death from Zika virus infections.Mechanism of splenic cell death and host mortality in a Plasmodium yoelii malaria model.Perforin Expression by CD8 T Cells Is Sufficient To Cause Fatal Brain Edema during Experimental Cerebral Malaria.Plasmodium attenuation: connecting the dots between early immune responses and malaria disease severity Spatiotemporal requirements for IRF7 in mediating type I IFN-dependent susceptibility to blood-stage Plasmodium infection.

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Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

http://www.wikidata.org/entity/Q37040808

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 16 May 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@en

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@nl

type

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Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@en

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@nl

prefLabel

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@en

Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

@nl

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EMBO Molecular Medicine

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Brain microvessel cross-presentation is a hallmark of experimental cerebral malaria.

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Chek Meng Poh

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Florent Ginhoux

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Gijsbert M Grotenbreg

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Nilabh Shastri

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P2860

Cerebral malaria: mysteries at the blood-brain barrier

Genome sequence and comparative analysis of the model rodent malaria parasite Plasmodium yoelii yoelii

IMGT/V-QUEST: the highly customized and integrated system for IG and TR standardized V-J and V-D-J sequence analysis

The role of animal models for research on severe malaria

Discovery of CD8+ T cell epitopes in Chlamydia trachomatis infection through use of caged class I MHC tetramers

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

Plasmodium falciparum adhesion on human brain microvascular endothelial cells involves transmigration-like cup formation and induces opening of intercellular junctions.

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

Directional, seamless, and restriction enzyme-free construction of random-primed complementary DNA libraries using phosphorothioate-modified primers.

Age-related differences in naturally acquired T cell memory to Plasmodium falciparum merozoite surface protein 1

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984-999

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scholarly article

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10.1002/EMMM.201202273

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7

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5

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Benoit Malleret

Shanshan W. Howland

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2013-05-16T00:00:00Z

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236916183

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23681698

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cerebral malaria

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3721469

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