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IL-10: The Master Regulator of Immunity to Infection

The Journal of immunology (1950), 2008-05, Vol.180 (9), p.5771-5777

2008

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IL-33-mediated protection against experimental cerebral malaria is linked to induction of type 2 innate lymphoid cells, M2 macrophages and regulatory T cells

PLoS pathogens, 2015-02, Vol.11 (2), p.e1004607-21

2015

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A quantitative brain map of experimental cerebral malaria pathology

PLoS pathogens, 2017-03, Vol.13 (3), p.e1006267-e1006267

2017

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Parasite-derived plasma microparticles contribute significantly to malaria infection-induced inflammation through potent macrophage stimulation

PLoS pathogens, 2010-01, Vol.6 (1), p.e1000744-e1000744

2010

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Plasmodium falciparum-infected erythrocyte co-culture with the monocyte cell line THP-1 does not trigger production of soluble factors reducing brain microvascular barrier function

PloS one, 2023-05, Vol.18 (5), p.e0285323-e0285323

2023

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The CTLA-4 and PD-1/PD-L1 inhibitory pathways independently regulate host resistance to Plasmodium-induced acute immune pathology

PLoS pathogens, 2012-02, Vol.8 (2), p.e1002504-e1002504

2012

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Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria

PLoS pathogens, 2015-11, Vol.11 (11), p.e1005210-e1005210

2015

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Lymphatic network drainage resolves cerebral edema and facilitates recovery from experimental cerebral malaria

Cell reports (Cambridge), 2024-05, Vol.43 (5), p.114217, Article 114217

2024

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Comparison of CD8 + T Cell Accumulation in the Brain During Human and Murine Cerebral Malaria

Frontiers in immunology, 2019-07, Vol.10, p.1747-1747

2019

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The Essential Role Played by B Cells in Supporting Protective Immunity Against Trichuris muris Infection Is by Controlling the Th1/Th2 Balance in the Mesenteric Lymph Nodes and Depends on Host Genetic Background

Frontiers in immunology, 2019-12, Vol.10, p.2842-2842

2019

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Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments

Infection and immunity, 2017-11, Vol.85 (11)

2017

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Cerebral malaria: why experimental murine models are required to understand the pathogenesis of disease

Parasitology, 2010-04, Vol.137 (5), p.755-772

2010

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The plasma membrane calcium ATPase 4 does not influence parasite levels but partially promotes experimental cerebral malaria during murine blood stage malaria

Malaria journal, 2021-07, Vol.20 (1), p.297-297, Article 297

2021

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IL-10 from CD4CD25Foxp3CD127 adaptive regulatory T cells modulates parasite clearance and pathology during malaria infection

PLoS pathogens, 2008-02, Vol.4 (2), p.e1000004-e1000004

2008

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Essential role for IL-27 receptor signaling in prevention of Th1-mediated immunopathology during malaria infection

The Journal of immunology (1950), 2010-08, Vol.185 (4), p.2482-2492

2010

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Treatment with specific and pan-plasma membrane calcium ATPase (PMCA) inhibitors reduces malaria parasite growth in vitro and in vivo

Malaria journal, 2022-06, Vol.21 (1), p.1-206, Article 206

2022

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IL-27 receptor signalling restricts the formation of pathogenic, terminally differentiated Th1 cells during malaria infection by repressing IL-12 dependent signals

PLoS pathogens, 2013-04, Vol.9 (4), p.e1003293-e1003293

2013

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IL-27 Receptor Signaling Regulates Memory CD4+ T Cell Populations and Suppresses Rapid Inflammatory Responses during Secondary Malaria Infection

Infection and Immunity, 2014-01, Vol.82 (1), p.10-20

2014

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Infection-Induced Resistance to Experimental Cerebral Malaria Is Dependent Upon Secreted Antibody-Mediated Inhibition of Pathogenic CD8 + T Cell Responses

Frontiers in immunology, 2019-02, Vol.10, p.248-248

2019

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The NLRP3 inflammasome as a target for sensorineural hearing loss

Clinical immunology (Orlando, Fla.), 2023-04, Vol.249, p.109287-109287, Article 109287

2023

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Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave of Plasmodium yoelii Parasitemia

Infection and Immunity, 2007-12, Vol.75 (12), p.5806-5818

2007

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WSX-1 signalling inhibits CD4⁺ T cell migration to the liver during malaria infection by repressing chemokine-independent pathways

PloS one, 2013-11, Vol.8 (11), p.e78486-e78486

2013

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Synergistic blockade of TIGIT and PD-L1 increases type-1 inflammation and improves parasite control during murine blood-stage Plasmodium yoelii non-lethal infection

Infection and immunity, 2024-09, Vol.92 (11)

2024

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IFN-γ-producing CD4+ T cells promote experimental cerebral malaria by modulating CD8+ T cell accumulation within the brain

The Journal of immunology (1950), 2012-07, Vol.189 (2), p.968-979

2012

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Increased Circulating Chemokines and Macrophage Recruitment in Growing Vestibular Schwannomas

Neurosurgery, 2023-03, Vol.92 (3), p.581-589

2023

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IL-10: The Master Regulator of Immunity to Infection

IL-33-mediated protection against experimental cerebral malaria is linked to induction of type 2 innate lymphoid cells, M2 macrophages and regulatory T cells

A quantitative brain map of experimental cerebral malaria pathology

Parasite-derived plasma microparticles contribute significantly to malaria infection-induced inflammation through potent macrophage stimulation

Plasmodium falciparum-infected erythrocyte co-culture with the monocyte cell line THP-1 does not trigger production of soluble factors reducing brain microvascular barrier function

The CTLA-4 and PD-1/PD-L1 inhibitory pathways independently regulate host resistance to Plasmodium-induced acute immune pathology

Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria

Lymphatic network drainage resolves cerebral edema and facilitates recovery from experimental cerebral malaria

Comparison of CD8 + T Cell Accumulation in the Brain During Human and Murine Cerebral Malaria

The Essential Role Played by B Cells in Supporting Protective Immunity Against Trichuris muris Infection Is by Controlling the Th1/Th2 Balance in the Mesenteric Lymph Nodes and Depends on Host Genetic Background

Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments

Cerebral malaria: why experimental murine models are required to understand the pathogenesis of disease

The plasma membrane calcium ATPase 4 does not influence parasite levels but partially promotes experimental cerebral malaria during murine blood stage malaria

IL-10 from CD4CD25Foxp3CD127 adaptive regulatory T cells modulates parasite clearance and pathology during malaria infection

Essential role for IL-27 receptor signaling in prevention of Th1-mediated immunopathology during malaria infection

Treatment with specific and pan-plasma membrane calcium ATPase (PMCA) inhibitors reduces malaria parasite growth in vitro and in vivo

IL-27 receptor signalling restricts the formation of pathogenic, terminally differentiated Th1 cells during malaria infection by repressing IL-12 dependent signals

IL-27 Receptor Signaling Regulates Memory CD4+ T Cell Populations and Suppresses Rapid Inflammatory Responses during Secondary Malaria Infection

Infection-Induced Resistance to Experimental Cerebral Malaria Is Dependent Upon Secreted Antibody-Mediated Inhibition of Pathogenic CD8 + T Cell Responses

The NLRP3 inflammasome as a target for sensorineural hearing loss

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave of Plasmodium yoelii Parasitemia

WSX-1 signalling inhibits CD4⁺ T cell migration to the liver during malaria infection by repressing chemokine-independent pathways

Synergistic blockade of TIGIT and PD-L1 increases type-1 inflammation and improves parasite control during murine blood-stage Plasmodium yoelii non-lethal infection

IFN-γ-producing CD4+ T cells promote experimental cerebral malaria by modulating CD8+ T cell accumulation within the brain

Increased Circulating Chemokines and Macrophage Recruitment in Growing Vestibular Schwannomas

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