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Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?Role of Trypanosoma cruzi Trans-sialidase on the Escape from Host Immune SurveillanceTrypanosoma cruzi Experimental Infection Impacts on the Thymic Regulatory T Cell CompartmentTrypanosoma cruzi disrupts thymic homeostasis by altering intrathymic and systemic stress-related endocrine circuitriesTNF-α is involved in the abnormal thymocyte migration during experimental Trypanosoma cruzi infection and favors the export of immature cellsEarly double-negative thymocyte export in Trypanosoma cruzi infection is restricted by sphingosine receptors and associated with human chagas disease.Tumor necrosis factor-α regulates glucocorticoid synthesis in the adrenal glands of Trypanosoma cruzi acutely-infected mice. the role of TNF-R1.Trypanosoma cruzi Infection through the Oral Route Promotes a Severe Infection in Mice: New Disease Form from an Old Infection?Neuroendocrine-immunology of experimental Chagas' disease.Extrathymic CD4+CD8+ lymphocytes in Chagas disease: possible relationship with an immunoendocrine imbalance.Oral immunization with live Lactococcus lactis expressing rotavirus VP8 subunit induces specific immune response in mice.Death of adrenocortical cells during murine acute T. cruzi infection is not associated with TNF-R1 signaling but mostly with the type II pathway of Fas-mediated apoptosis.The sympathetic nervous system affects the susceptibility and course of Trypanosoma cruzi infection.Efficacy of a trans-sialidase-ISCOMATRIX subunit vaccine candidate to protect against experimental Chagas disease.Immunoendocrine dysbalance during uncontrolled T. cruzi infection is associated with the acquisition of a Th-1-like phenotype by Foxp3(+) T cells.Trans-sialidase-based vaccine candidate protects against Trypanosoma cruzi infection, not only inducing an effector immune response but also affecting cells with regulatory/suppressor phenotype.Reciprocal influences between leptin and glucocorticoids during acute Trypanosoma cruzi infection.Thymus atrophy during Trypanosoma cruzi infection is caused by an immuno-endocrine imbalance.Immunoneuroendocrine alterations in patients with progressive forms of chronic Chagas disease.Short treatment with the tumour necrosis factor-alpha blocker infliximab diminishes chronic chagasic myocarditis in rats without evidence of Trypanosoma cruzi reactivation.Role of Hormonal Circuitry Upon T Cell Development in Chagas Disease: Possible Implications on T Cell Dysfunctions.Immune response triggered by Trypanosoma cruzi infection strikes adipose tissue homeostasis altering lipid storage, enzyme profile and adipokine expressionGenetic Engineering of Co-producing Antigen and the Mucosal Adjuvant 3' 5'- cyclic di Adenosine Monophosphate (c-di-AMP) as a Design Strategy to Develop a Mucosal Vaccine PrototypeA high corticosterone/DHEA-s ratio in young rats infected with Trypanosoma cruzi is associated with increased susceptibilityImmunoendocrinology of the thymus in Chagas diseaseImproved outcome of Trypanosoma cruzi infection in rats following treatment in early life with suspensions of heat-killed environmental ActinomycetalesEndogenous glucocorticoids cause thymus atrophy but are protective during acute Trypanosoma cruzi infectionDeficient control of Trypanosoma cruzi infection in C57BL/6 mice is related to a delayed specific IgG response and increased macrophage production of pro-inflammatory cytokinesDysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas CardiomyopathyImmune-endocrine interactions related to a high risk of infections in chronic metabolic diseases: The role of PPAR gamma
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description
investigador
@es
researcher
@en
wetenschapper
@nl
name
Ana Rosa Perez
@en
Perez AR
@nl
type
label
Ana Rosa Perez
@en
Perez AR
@nl
altLabel
Perez AR
@en
prefLabel
Ana Rosa Perez
@en
Perez AR
@nl
P31
P496
0000-0002-1636-7523