Q3137676 (Q3137676): Difference between revisions
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(Changed an Item: Edited by the materialized bot - inferring region from the coordinates) |
(Created claim: summary (P836): Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The disease has a major impact on the quality of life of patients and their families. The etiology of the disease is unknown, but it is known that there is a complex interaction between genetic and environmental factors. DNA methylation moderates gen-environmental interactions and provides stable and hereditary epigenetic regulation. Changes in methylo...) |
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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The disease has a major impact on the quality of life of patients and their families. The etiology of the disease is unknown, but it is known that there is a complex interaction between genetic and environmental factors. DNA methylation moderates gen-environmental interactions and provides stable and hereditary epigenetic regulation. Changes in methyloma have been observed in different autoimmune diseases. Our hypothesis is that changes in the methylation of regulatory T cells (CD4+/Foxp3+) and B cells (CD19+) may be involved in the debut and progression of disease and in response to specific treatments. We have selected regulator T cells and B cells because they have been shown to be overactivated in MS. B cells play an important role in the onset and maintenance of inflammation in CNS, while regulatory T cells have a key function as regulators of self-reactivity and inflammatory response and induce immunotolerance. We would like to emphasise that this project differs from other methylation projects in MS due to two important factors: (1) Our study will not be carried out in a pool of different cell types, but in a homogeneous cell group of regulator T cells on one side and B cells on the other, and (2) We will validate the changes found by a transcriptome study. (English) | |||||||||||||||
| Property / summary: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The disease has a major impact on the quality of life of patients and their families. The etiology of the disease is unknown, but it is known that there is a complex interaction between genetic and environmental factors. DNA methylation moderates gen-environmental interactions and provides stable and hereditary epigenetic regulation. Changes in methyloma have been observed in different autoimmune diseases. Our hypothesis is that changes in the methylation of regulatory T cells (CD4+/Foxp3+) and B cells (CD19+) may be involved in the debut and progression of disease and in response to specific treatments. We have selected regulator T cells and B cells because they have been shown to be overactivated in MS. B cells play an important role in the onset and maintenance of inflammation in CNS, while regulatory T cells have a key function as regulators of self-reactivity and inflammatory response and induce immunotolerance. We would like to emphasise that this project differs from other methylation projects in MS due to two important factors: (1) Our study will not be carried out in a pool of different cell types, but in a homogeneous cell group of regulator T cells on one side and B cells on the other, and (2) We will validate the changes found by a transcriptome study. (English) / rank | |||||||||||||||
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| Property / summary: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The disease has a major impact on the quality of life of patients and their families. The etiology of the disease is unknown, but it is known that there is a complex interaction between genetic and environmental factors. DNA methylation moderates gen-environmental interactions and provides stable and hereditary epigenetic regulation. Changes in methyloma have been observed in different autoimmune diseases. Our hypothesis is that changes in the methylation of regulatory T cells (CD4+/Foxp3+) and B cells (CD19+) may be involved in the debut and progression of disease and in response to specific treatments. We have selected regulator T cells and B cells because they have been shown to be overactivated in MS. B cells play an important role in the onset and maintenance of inflammation in CNS, while regulatory T cells have a key function as regulators of self-reactivity and inflammatory response and induce immunotolerance. We would like to emphasise that this project differs from other methylation projects in MS due to two important factors: (1) Our study will not be carried out in a pool of different cell types, but in a homogeneous cell group of regulator T cells on one side and B cells on the other, and (2) We will validate the changes found by a transcriptome study. (English) / qualifier | |||||||||||||||
point in time: 12 October 2021
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Revision as of 13:05, 12 October 2021
Project Q3137676 in Spain
| Language | Label | Description | Also known as |
|---|---|---|---|
| English | No label defined |
Project Q3137676 in Spain |
Statements
30,750.0 Euro
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61,500.0 Euro
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50.0 percent
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1 January 2017
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31 March 2020
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FUNDACION INSTITUTO DE INVESTIGACION BIOMEDICA DE GERONA
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41°58'45.48"N, 2°49'11.78"E
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17079
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La esclerosis múltiple (EM) es una enfermedad crónica inflamatoria del sistema nervioso central (SNC). La enfermedad produce un gran impacto en la calidad de vida de los pacientes y de sus familias. La etiología de la enfermedad es desconocida, pero se sabe que existe una compleja interacción entre factores genéticos y ambientales. La metilación del DNA modera las interacciones gen-ambiente y proporciona una regulación epigenética estable y heredable. Se han observado cambios en el metiloma en diferentes enfermedades autoinmunes. Nuestra hipótesis es que cambios en la metilación de células T reguladoras (CD4+/Foxp3+) y células B (CD19+) pueden estar implicados en el debut y la progresión de la enfermerdad y en la respuesta a los tratamientos específicos. Hemos seleccionado las células T reguladoras y las células B porque se ha demostrado que están sobreactivadas en la EM. Las células B juegan un importante papel en el inicio y el mantenimiento de la inflamación en el SNC, mientras que las células T reguladoras tienen una función clave como reguladoras de la autoreactividad y de la respuesta inflamatoria e inducen la inmunotolerancia. Queremos destacar que este proyecto difiere de otros proyectos de metilaciones en EM por dos importantes factores: (1) Nuestro estudio no se realizará en un pool de diferentes tipos celulares, sinó en un grupo celular homogéneo de células T reguladoras por un lado y de células B por el otro, y (2) Validaremos los cambios hallados mediante un estudio de transcriptoma (Spanish)
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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). The disease has a major impact on the quality of life of patients and their families. The etiology of the disease is unknown, but it is known that there is a complex interaction between genetic and environmental factors. DNA methylation moderates gen-environmental interactions and provides stable and hereditary epigenetic regulation. Changes in methyloma have been observed in different autoimmune diseases. Our hypothesis is that changes in the methylation of regulatory T cells (CD4+/Foxp3+) and B cells (CD19+) may be involved in the debut and progression of disease and in response to specific treatments. We have selected regulator T cells and B cells because they have been shown to be overactivated in MS. B cells play an important role in the onset and maintenance of inflammation in CNS, while regulatory T cells have a key function as regulators of self-reactivity and inflammatory response and induce immunotolerance. We would like to emphasise that this project differs from other methylation projects in MS due to two important factors: (1) Our study will not be carried out in a pool of different cell types, but in a homogeneous cell group of regulator T cells on one side and B cells on the other, and (2) We will validate the changes found by a transcriptome study. (English)
12 October 2021
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Girona
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Identifiers
PI16_01140
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