Th2 but not Th1 immune bias results in altered lung functions in a murine model of pulmonary Cryptococcus neoformans infection. - Wikidata - awgldk - TriplyDB

Th2 but not Th1 immune bias results in altered lung functions in a murine model of pulmonary Cryptococcus neoformans infection.

Th2 but not Th1 immune bias results in altered lung functions in a murine model of pulmonary Cryptococcus neoformans infection.

http://www.wikidata.org/entity/Q37451004

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Cryptococcus and Phagocytes: Complex Interactions that Influence Disease Outcome Adaptive immunity to fungi Lack of IL-4 receptor expression on T helper cells reduces T helper 2 cell polyfunctionality and confers resistance in allergic bronchopulmonary mycosis Scavenger receptor A modulates the immune response to pulmonary Cryptococcus neoformans infection.Cryptococcus neoformans hyperfilamentous strain is hypervirulent in a murine model of cryptococcal meningoencephalitis.TLR9 signaling is required for generation of the adaptive immune protection in Cryptococcus neoformans-infected lungs.STAT1 signaling is essential for protection against Cryptococcus neoformans infection in mice.Interleukin-17 is not required for classical macrophage activation in a pulmonary mouse model of Cryptococcus neoformans infection.Immune modulation mediated by cryptococcal laccase promotes pulmonary growth and brain dissemination of virulent Cryptococcus neoformans in mice.Eosinophils contribute to IL-4 production and shape the T-helper cytokine profile and inflammatory response in pulmonary cryptococcosis.Chitin recognition via chitotriosidase promotes pathologic type-2 helper T cell responses to cryptococcal infection.Critical role for IL-18 in spontaneous lung inflammation caused by autophagy deficiency.Cryptococcal heat shock protein 70 homolog Ssa1 contributes to pulmonary expansion of Cryptococcus neoformans during the afferent phase of the immune response by promoting macrophage M2 polarization Antibodies to Pseudogymnoascus destructans are not sufficient for protection against white-nose syndrome.IL-23 dampens the allergic response to Cryptococcus neoformans through IL-17-independent and -dependent mechanisms.Vaccine and immunotherapeutic approaches for the prevention of cryptococcosis: lessons learned from animal models.Cryptococcal genotype influences immunologic response and human clinical outcome after meningitis.STAT1 signaling within macrophages is required for antifungal activity against Cryptococcus neoformans The Cnes2 locus on mouse chromosome 17 regulates host defense against cryptococcal infection through pleiotropic effects on host immunity Virulence factors identified by Cryptococcus neoformans mutant screen differentially modulate lung immune responses and brain dissemination.Cryptococcus neoformans Rim101 is associated with cell wall remodeling and evasion of the host immune responses.Cryptococcus neoformans growth and protection from innate immunity are dependent on expression of a virulence-associated DEAD-box protein, Vad1.Macrophage M1/M2 polarization dynamically adapts to changes in cytokine microenvironments in Cryptococcus neoformans infection.X-linked immunodeficient mice exhibit enhanced susceptibility to Cryptococcus neoformans Infection.DAP12 Inhibits Pulmonary Immune Responses to Cryptococcus neoformans The intracellular life of Cryptococcus neoformans.IL-4 receptor-alpha-dependent control of Cryptococcus neoformans in the early phase of pulmonary infection.Impact of surfactant protein D, interleukin-5, and eosinophilia on Cryptococcosis.Mechanisms of cryptococcal virulence and persistence.Induction of protective immunity against cryptococcosis.Cryptococcus antigens and immune responses: implications for a vaccine.Immunity to Cryptococcus neoformans and C. gattii during cryptococcosis Innate host defenses against Cryptococcus neoformans.T Cell-Restricted Notch Signaling Contributes to Pulmonary Th1 and Th2 Immunity during Cryptococcus neoformans Infection.Analysis of asthma patients for cryptococcal seroreactivity in an urban German area.Innate Immune Responses to Cryptococcus.Dietary vitamin D3 deficiency exacerbates sinonasal inflammation and alters local 25(OH)D3 metabolism.CD4+ T Cells Orchestrate Lethal Immune Pathology despite Fungal Clearance during Cryptococcus neoformans Meningoencephalitis.The F-Box Protein Fbp1 Shapes the Immunogenic Potential of Cryptococcus neoformans.Anti-PD-1 Antibody Treatment Promotes Clearance of Persistent Cryptococcal Lung Infection in Mice.

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Th2 but not Th1 immune bias results in altered lung functions in a murine model of pulmonary Cryptococcus neoformans infection.

http://www.wikidata.org/entity/Q37451004

description

article científic

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article scientifique

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artigo científico

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bilimsel makale

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scientific article published on 14 September 2009

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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

Th2 but not Th1 immune bias re ...... tococcus neoformans infection.

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Th2 but not Th1 immune bias re ...... tococcus neoformans infection.

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Th2 but not Th1 immune bias re ...... tococcus neoformans infection.

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Th2 but not Th1 immune bias re ...... tococcus neoformans infection.

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Th2 but not Th1 immune bias re ...... tococcus neoformans infection.

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Infection and Immunity

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Th2 but not Th1 immune bias re ...... ptococcus neoformans infection

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Aditya V Jain

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Galen B Toews

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Gary B Huffnagle

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Gwo-Hsiao Chen

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John Erb-Downward

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John J Osterholzer

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Mun Y Choe

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W Bradley Fields

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Yanmei Zhang

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P2860

A causative relationship exists between eosinophils and the development of allergic pulmonary pathologies in the mouse

CCR2 expression determines T1 versus T2 polarization during pulmonary Cryptococcus neoformans infection

Proinflammatory and Th2 cytokines regulate the high affinity IgE receptor (FcepsilonRI) and IgE-dependant activation of human airway smooth muscle cells

The late, but not early, asthmatic response is dependent on IL-5 and correlates with eosinophil infiltration.

Requirement for CD4(+) T lymphocytes in host resistance against Cryptococcus neoformans in the central nervous system of immunized mice.

Anti-IgE therapy in asthma: rationale and therapeutic potential.

Pulmonary T cells and eosinophils: coconspirators or independent triggers of allergic respiratory pathology?

Effect of a CD4-depleting antibody on the development of Cryptococcus neoformans-induced allergic bronchopulmonary mycosis in mice.

Interleukins-4, -5, and -13: emerging therapeutic targets in allergic disease.

A role for CD44 in an antigen-induced murine model of pulmonary eosinophilia.

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5389-5399

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10.1128/IAI.00809-09

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12

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Michal Olszewski

David A McNamara

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2009-09-14T00:00:00Z

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