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The role of parasite persistence in pathogenesis of Chagas heart disease.

The role of parasite persistence in pathogenesis of Chagas heart disease.

http://www.wikidata.org/entity/Q37613774

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Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?Evasion of the Immune Response by Trypanosoma cruzi during Acute Infection Immune Evasion Strategies of Trypanosoma cruzi Mechanisms of Trypanosoma cruzi persistence in Chagas disease A new experimental model for assessing drug efficacy against Trypanosoma cruzi infection based on highly sensitive in vivo imaging Modulation of Trypanosoma cruzi-specific T-cell responses after chemotherapy for chronic Chagas disease Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease Differential trypanocidal activity of novel macrolide antibiotics; correlation to genetic lineage Pathogenesis of chagas' disease: parasite persistence and autoimmunity Coronary microvascular disease in chronic Chagas cardiomyopathy including an overview on history, pathology, and other proposed pathogenic mechanisms.Epidemiological modeling of Trypanosoma cruzi: Low stercorarian transmission and failure of host adaptive immunity explain the frequency of mixed infections in humans Trypanosoma cruzi in the chicken model: Chagas-like heart disease in the absence of parasitism.Subdominant/cryptic CD8 T cell epitopes contribute to resistance against experimental infection with a human protozoan parasite.Benzonidazole therapy modulates interferon-γ and M2 muscarinic receptor autoantibody responses in Trypanosoma cruzi-infected children.Crucial role of the central leptin receptor in murine Trypanosoma cruzi (Brazil strain) infection Cardiac-oxidized antigens are targets of immune recognition by antibodies and potential molecular determinants in chagas disease pathogenesis.Effects of cholinergic stimulation with pyridostigmine bromide on chronic chagasic cardiomyopathic mice.Interferon-γ and other inflammatory mediators in cardiomyocyte signaling during Chagas disease cardiomyopathy.Importance of nonenteric protozoan infections in immunocompromised people.Pathogen-induced proapoptotic phenotype and high CD95 (Fas) expression accompany a suboptimal CD8+ T-cell response: reversal by adenoviral vaccine.Tc52 amino-terminal-domain DNA carried by attenuated Salmonella enterica serovar Typhimurium induces protection against a Trypanosoma cruzi lethal challenge.Bioluminescence imaging of chronic Trypanosoma cruzi infections reveals tissue-specific parasite dynamics and heart disease in the absence of locally persistent infection.Early double-negative thymocyte export in Trypanosoma cruzi infection is restricted by sphingosine receptors and associated with human chagas disease.Low doses of simvastatin therapy ameliorate cardiac inflammatory remodeling in Trypanosoma cruzi-infected dogs.Cell death and serum markers of collagen metabolism during cardiac remodeling in Cavia porcellus experimentally infected with Trypanosoma cruzi Evaluating Chagas disease progression and cure through blood-derived biomarkers: a systematic review.Inhibitory effects of Trypanosoma cruzi sialoglycoproteins on CD4+ T cells are associated with increased susceptibility to infection Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection MIF synergizes with Trypanosoma cruzi antigens to promote efficient dendritic cell maturation and IL-12 production via p38 MAPK.Trypanosoma cruzi Infection through the Oral Route Promotes a Severe Infection in Mice: New Disease Form from an Old Infection?Genetic Susceptibility to Cardiac and Digestive Clinical Forms of Chronic Chagas Disease: Involvement of the CCR5 59029 A/G Polymorphism.Inflammation Enhances the Risks of Stroke and Death in Chronic Chagas Disease Patients.GRAIL and Otubain-1 are Related to T Cell Hyporesponsiveness during Trypanosoma cruzi Infection Host metabolism regulates intracellular growth of Trypanosoma cruzi.Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells Evaluation of VDR gene polymorphisms in Trypanosoma cruzi infection and chronic Chagasic cardiomyopathy.Host and parasite genetics shape a link between Trypanosoma cruzi infection dynamics and chronic cardiomyopathy Accelerating the development of a therapeutic vaccine for human Chagas disease: rationale and prospects Epitope Capsid-Incorporation: New Effective Approach for Vaccine Development for Chagas Disease.Chemotherapeutic efficacy of phosphodiesterase inhibitors in chagasic cardiomyopathy.

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The role of parasite persistence in pathogenesis of Chagas heart disease.

http://www.wikidata.org/entity/Q37613774

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2009 nî lūn-bûn

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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2009年學術文章

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2009年學術文章

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name

The role of parasite persistence in pathogenesis of Chagas heart disease.

@en

The role of parasite persistence in pathogenesis of Chagas heart disease.

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type

label

The role of parasite persistence in pathogenesis of Chagas heart disease.

@en

The role of parasite persistence in pathogenesis of Chagas heart disease.

@nl

prefLabel

The role of parasite persistence in pathogenesis of Chagas heart disease.

@en

The role of parasite persistence in pathogenesis of Chagas heart disease.

@nl

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J.1365-3024.2009.01108.X

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Parasite Immunology

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The role of parasite persistence in pathogenesis of Chagas heart disease.

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F R S Gutierrez

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J S Silva

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P M M Guedes

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R T Gazzinelli

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P2860

Modulation of chemokine production and inflammatory responses in interferon-gamma- and tumor necrosis factor-R1-deficient mice during Trypanosoma cruzi infection.

Interleukin-17 as an effector molecule of innate and acquired immunity against infections.

Stable CD8+ T cell memory during persistent Trypanosoma cruzi infection.

Autoimmune myocarditis induced by Trypanosoma cruzi.

Human T cells that are able to produce IL-17 express the chemokine receptor CCR6.

Natural and induced CD4+CD25+ cells educate CD4+CD25- cells to develop suppressive activity: the role of IL-2, TGF-beta, and IL-10.

Nitric oxide induces upregulation of Fas and apoptosis in vascular smooth muscle.

Expression of functional TLR4 confers proinflammatory responsiveness to Trypanosoma cruzi glycoinositolphospholipids and higher resistance to infection with T. cruzi.

[Human activities and American trypanosomiasis. Review of the literature].

Nova tripanozomiaze humana: estudos sobre a morfolojia e o ciclo evolutivo do Schizotrypanum cruzi n. gen., n. sp., ajente etiolojico de nova entidade morbida do homem

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