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  1. Home
  2. Browse by Author

Browsing by Author "Iruretagoyena B., Mirentxu"

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    Activating and inhibitory Fc gamma receptors can differentially modulate T cell-mediated autoimmunity
    (2008) Iruretagoyena B., Mirentxu; Riedel Soria, Claudia; Leiva Llantén, Eduardo David; Gutiérrez Torres, Miguel Alejandro; Jacobelli, Sergio H.; Kalergis Parra, Alexis Mikes
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    Andrographolide Interferes With T Cell Activation and Reduces Experimental Autoimmune Encephalomyelitis in the Mouse
    (2005) Iruretagoyena B., Mirentxu; Kalergis Parra, Alexis Mikes
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    Clusters of Autoimmune Diseases in Children and the Role of PTPN22 C1858T Gene Polymorphism in Pediatric Polyautoimmunity
    (2014) Borzutzky Schachter, Arturo; Seiltgens, Cristián; Iruretagoyena B., Mirentxu; Cristi, Francisca; Ponce, María Jesús ; Melendez, Patricia; Martínez Aguayo, Alejandro; Hodgson Bunster, María Isabel; Talesnik Guendelman, Eduardo; Riera Cassorla, Francisca Paz; Méndez, Cecilia; Harris D., Paul R.; García Bruce, Hernán; Gana Ansaldo, Juan Cristóbal; Godoy, Claudia; Cattani Ortega, Andreína
    Background/Purpose:Autoimmune diseases (AIDs) have familial aggregation and frequently share a common genetic background, but few studies have evaluated autoimmune clusters in children with AIDs and their families. Children with more than one AID (pediatric polyautoimmunity) may have a stronger genetic component than children with a single AID. The objectives of this study were to identify clusters of AIDs in children and their first-degree relatives and to evaluate the association of PTPN22 C1858T gene polymorphism with pediatric polyautoimmunity.Methods:A cross-sectional study was performed in subjects with an AID of pediatric onset (<18 years)recruited at Pediatric Rheumatology, Endocrinology and Gastroenterology Clinics at the Health Network of the Pontificia Universidad Católica de Chile School of Medicine. Clusters of AIDs were identified by K-means cluster analysis. The PTPN22 C1858T gene polymorphism was determined by RT-PCR in subjects with pediatric polyautoimmunity and in subjects with three common AIDs: juvenile idiopathic arthritis (JIA), autoimmune thyroid disease (AITD), and type I diabetes (T1D).Results:191 subjects with pediatric AIDs were included, of which 45 (24%) had polyautoimmunity. Mean age was 12.1 years (range 1–19) and 68% were female. Most frequent AIDs were JIA (36%), AITD (25%), T1D (19%), uveitis (8%), celiac disease (6%), and vitiligo (6%). 59% of subjects with pediatric autoimmunity had first-degree relatives with an AID. Five clusters of AID were identified in families of children with autoimmunity (Table 1). Among the 45 subjects with pediatric polyautoimmunity, four clusters of AIDs were identified (Table 2). Genomic DNA from 128 subjects was evaluated for PTPN22 C1858T gene polymorphism revealing common homozygosity (C/C) in 85.2%, heterozygosity (C/T) in 13.3%, and rare homozygosity (T/T) in 1.6 %, in equilibrium with Hardy Weinberg equation (P = 0.4). 26% of polyautoimmune subjects had the T allele in contrast with 11% of monoautoimmune subjects (P = 0.04). No significant difference was found in the age of onset of autoimmunity between mono and polyautoimmune subjects (P = 0.44) or between subjects with C/C genotype vs. C/T and T/T genotypes (P = 0.81).
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    Comparison of Health-Related Quality of Life in Chilean Patients with Systemic Lupus Erythematosus, Rheumatoid Arthritis and Systemic Sclerosis
    (2015) Iruretagoyena B., Mirentxu; Hirigoyen, D.; Naves, R.; Juacida, N.; Álvarez Rojas, Alejandra; Villarroel del Pino, Luis A.
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    Compromiso renal en vasculitis asociadas a anticuerpos anticitoplasma de neutrófilos. Recomendaciones de consenso de las Sociedades Chilenas de Nefrología y Reumatología
    (2018) Aguirre, Verónica; Alvo, Miriam; Ardiles, Leopoldo; Fierro, Alberto; Goecke, Annelise; Iruretagoyena B., Mirentxu; Jalil Milad, Roberto; Massardo Vega, Loreto; Méndez Olivieri, Gonzalo Patricio; Palma, Sergio; Roessler, Emilio; Silva, Francisco; Wurgaft, Andrés
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    Entrenamiento microquirúrgico básico para realizar un modelo animal de alotrasplante compuesto vascularizado
    (2013) Ramírez, Alejandro E.; Contreras Darvas, Rodrigo Alejandro; Cartes Urenda, Jaime Andrés; Martínez M., Mónica; Martínez P., Carlos; Alvarado, Valeria; Iruretagoyena B., Mirentxu; Martínez Castillo, Jorge
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    Esofagitis eosinofílica : Diagnóstico y manejo
    (2020) Ballart, M. J.; Monrroy Bravo, Hugo Alfonso; Iruretagoyena B., Mirentxu; Parada Daza, Alejandra; Torres Montes, Paula Javiera; Espino Espino, Alberto Antonio
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    Hemicorea como primera manifestación clínica de lupus eritematoso sistémico
    (2017) Armstrong Bruzzone, Macarena; Iruretagoyena B., Mirentxu; Burgos, Paula I.
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    Hipoglicemia recurrente como causa reversible de síndrome demencial en adultos mayores diabéticos, a propósito de un caso
    (2010) Aizman, Andrés; Luis Manuel Sanhueza, A.; Iruretagoyena B., Mirentxu; Abbott Cáceres, Eduardo Francisco; Rodríguez, J.C.; Rojas Orellana, Luis
    We report a 78 year-old diabetic woman, treated with gliburide and metformin, consulting in the emergency room for a non fuctuating impairment in consciousness. She had a history of similar episodes in the last two months. A brain CAT scan showed an old putamen lacunar infarction. Noteworthy was the presence of a low glycosilated hemoglobin level of 5.2%. Hypoglycemic medications were discontinued and the patient was discharged in good conditions. After six months of follow up, the patient did not have further episodes of impairment of consciousness.
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    Inducción de tolerancia en modelo de autotrasplante
    (2015) Ramírez M., Alejandro; Iruretagoyena B., Mirentxu; Contreras D., Rodrigo; Cartes Urenda, Jaime Andrés; Martínez M., Mónica; Martínez M., Carlos; Alvarado S., Valeria; Martínez Castillo, Jorge
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    Inhibition of angiogenesis by platelets in systemic sclerosis patients
    (2015) Hirigoyen Pérez, Daniela María.; Burgos, Paula I.; Mezzano, Veronica.; Durán, Josefina; Barrientos, Magaly.; Sáez, Claudia G.; Panes Becerra, Olga Teresa; Mezzano, Diego; Iruretagoyena B., Mirentxu
    Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.
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    Inhibition of Nuclear Factor-κB Enhances the Capacity of Immature Dendritic Cells to Induce Antigen-Specific Tolerance in Experimental Autoimmune Encephalomyelitis
    (2006) Iruretagoyena B., Mirentxu; Bronfman A., Miguel L.; Kalergis Parra, Alexis Mikes
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    Interaction At the Dendritic Cell/T-Cell Interface Define the Balance Between Immunity and Tolerance
    (2005) Iruretagoyena B., Mirentxu; Kalergis Parra, Alexis Mikes
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    Role of dendritic cells in peanut allergy
    (2018) Aguilera, Raquel; Venegas, Luis F.; Iruretagoyena B., Mirentxu; Rojas Cortéz, Leticia Andrea; Borzutzky Schachter, Arturo
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    Role of Nrf2 in the regulation of the Mrp2 (ABCC2) gene
    (2006) Vollrath Reyes, Valeska.; Wielandt Necochea, Ana María.; Iruretagoyena B., Mirentxu; Chianale Bertolini, José Luis
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    Smoking promotes exacerbated inflammatory features in dendritic cells of Chilean rheumatoid arthritis patients
    (2018) Prado, Carolina; Iruretagoyena B., Mirentxu; Burgos, Paula I.; Pacheco, Rodrigo
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    The Dendritic Cell-T Cell Synapse As a Determinant of Autoimmune Pathogenesis
    (2006) Iruretagoyena B., Mirentxu; Kalergis Parra, Alexis Mikes
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    The prevalence of rheumatoid arthritis in Chile : a nationwide study performed as part of the national health survey
    (2020) Durán, Josefina; Massardo Vega, Loreto; Llanos Muñoz, Carolina; Iacobelli Gabrielli, Sergio Hernán; Burgos, Paula I.; Cisternas Martínez, Marcela Carolina; Iruretagoyena B., Mirentxu; Armstrong Bruzzone, Macarena; Aguilera Insunza, Raquel; Radrigán Araya, Francisco José Ricardo; Martínez Ruiz-Esquide, María Eugenia; Passi Solar, Alvaro Rodrigo; Vásquez Aravena, Nancy Margarita; Margozzini Maira, Paula; Riedemann, P.; Crisóstomo, N.; Cifuentes, C.; Hagedorn, L.; Cisternas, A.

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