Bradykinin B2 Receptors of dendritic cells, acting as sensors of kinins proteolytically released by Trypanosoma cruzi, are critical for the development of protective type-1 responses - Wikidata - wikimedia - TriplyDB

Bradykinin B2 Receptors of dendritic cells, acting as sensors of kinins proteolytically released by Trypanosoma cruzi, are critical for the development of protective type-1 responses

Bradykinin B2 Receptors of dendritic cells, acting as sensors of kinins proteolytically released by Trypanosoma cruzi, are critical for the development of protective type-1 responses

http://www.wikidata.org/entity/Q27319499

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Dendritic Cells: A Double-Edged Sword in Immune Responses during Chagas Disease Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease IL-17 produced during Trypanosoma cruzi infection plays a central role in regulating parasite-induced myocarditis Impaired innate immunity in Tlr4(-/-) mice but preserved CD8+ T cell responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-deficient mice.Immunoregulatory networks in human Chagas disease.Repertoire, genealogy and genomic organization of cruzipain and homologous genes in Trypanosoma cruzi, T. cruzi-like and other trypanosome species.Caspase-1/ASC inflammasome-mediated activation of IL-1β-ROS-NF-κB pathway for control of Trypanosoma cruzi replication and survival is dispensable in NLRP3-/- macrophages.Mannose-binding lectin regulates host resistance and pathology during experimental infection with Trypanosoma cruzi Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection Cruzipain Activates Latent TGF-β from Host Cells during T. cruzi Invasion.The Immune Response to Trypanosoma cruzi: Role of Toll-Like Receptors and Perspectives for Vaccine Development.Trypanosoma cruzi invades host cells through the activation of endothelin and bradykinin receptors: a converging pathway leading to chagasic vasculopathy.The kallikrein-kinin system as a regulator of cardiovascular and renal function.Resistance to visceral leishmaniasis is severely compromised in mice deficient of bradykinin B2-receptors.High interleukin 17 expression is correlated with better cardiac function in human Chagas disease.Perspectives on the Trypanosoma cruzi-host cell receptor interactions.Kinin danger signals proteolytically released by gingipain induce Fimbriae-specific IFN-gamma- and IL-17-producing T cells in mice infected intramucosally with Porphyromonas gingivalis.Back to the future in Chagas disease: from animal models to patient cohort studies, progress in immunopathogenesis research.The effects of nitric oxide on the immune system during Trypanosoma cruzi infection.Modulation of dendritic cell responses by parasites: a common strategy to survive.The role of Toll-like receptors and adaptive immunity in the development of protective or pathological immune response triggered by the Trypanosoma cruzi protozoan.Targeting the 'Janus face' of the B2-bradykinin receptor.Mast Cell Coupling to the Kallikrein-Kinin System Fuels Intracardiac Parasitism and Worsens Heart Pathology in Experimental Chagas Disease.Pathogenesis of Chagas disease: time to move on.Intracellular proteolysis of kininogen by malaria parasites promotes release of active kinins.Ecotin-like ISP of L. major promastigotes fine-tunes macrophage phagocytosis by limiting the pericellular release of bradykinin from surface-bound kininogens: a survival strategy based on the silencing of proinflammatory G-protein coupled kinin B2 a Nitric oxide synthase-2 modulates chemokine production by Trypanosoma cruzi-infected cardiac myocytes The kallikrein-kinin system in experimental Chagas disease: a paradigm to investigate the impact of inflammatory edema on GPCR-mediated pathways of host cell invasion by Trypanosoma cruzi.Increased bone loss and amount of osteoclasts in kinin B1 receptor knockout mice.Benznidazole affects expression of Th1, Th17 and Treg cytokines during acute experimental Trypanosoma cruzi infection.A novel locus on mouse chromosome 7 that influences survival after infection with tick-borne encephalitis virus.Captopril increases the intensity of monocyte infection by Trypanosoma cruzi and induces human T helper type 17 cells

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Bradykinin B2 Receptors of dendritic cells, acting as sensors of kinins proteolytically released by Trypanosoma cruzi, are critical for the development of protective type-1 responses

http://www.wikidata.org/entity/Q27319499

description

2007 nî lūn-bûn

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2007 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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Alessandra Granato

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Ana Carolina Monteiro

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Fnu Nagajyothi

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João B Pesquero

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Julio Scharfstein

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Luciana Barros de Arruda

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Verônica Schmitz

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P2860

Bioregulation of kinins: kallikreins, kininogens, and kininases

International union of pharmacology. XLV. Classification of the kinin receptor family: from molecular mechanisms to pathophysiological consequences

Transforming growth factor-beta induces development of the T(H)17 lineage

Pathogenesis of chronic Chagas heart disease

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

CD8+ T-Cell responses to Trypanosoma cruzi are highly focused on strain-variant trans-sialidase epitopes

Both CD1d antigen presentation and interleukin-12 are required to activate natural killer T cells during Trypanosoma cruzi infection

Type 1 chemokine receptor expression in Chagas' disease correlates with morbidity in cardiac patients.

Pathogenesis of periodontitis: a major arginine-specific cysteine proteinase from Porphyromonas gingivalis induces vascular permeability enhancement through activation of the kallikrein/kinin pathway.

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Werner Müller-Esterl

Alexandre Morrot

Herbert B Tanowitz

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Trypanosoma cruzi

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