AURELIE TRENADO · Role of Foxp3 in immune tolerance in EAE the murine model for multiple sclerosis
6РП — Действия „Мария Кюри“
- Период
- 2007-01-01 → 2009-10-31
- Финансиране от ЕС
- 261 050 €
- Участници
- 2
- Схема
- OIF
Линиите свързват координатора с партньорите. За проекти отпреди 2014 г. CORDIS не винаги дава точни координати. Тези точки са на ниво град или държава.
Накратко на български
Ролята на протеина Foxp3 при създаването на регулаторни Т-клетки се изучава чрез мишарски модел на рассеяната склероза. Разбирането на тези механизми помага да се разбере как имунната система толерира собствените тъкани и защо при някои пациенти тази защита отпада.
Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.
Цел на проекта
Multiple Sclerosis is the chronic neurological disease the most frequent in the young adult. This disease is characterized by an inflammatory attack of the central nervous system, which leads to the destruction of the myelin gain of the axon. The animal model of this disease, the EAE (experimental autoimmune encephalomyelitis) permitted to better characterize this auto-immune disease.More recently, the role of a specific population of lymphocytes the CD4+CD25+ regulatory T cells (Tregs) in the regulation of autoimmunity was brought to light. These cells were generated in the thymus and there is a decrease in the number and function of this class of regulatory T cells in Multiple Slerosis patients, suggesting that the loss of these cells promotes the induction and the persistence of the disease.In EAE, there is now considerable evidence that Tregs are involved in genetic resistance and in mediating remission of the disease. Thus understanding the molecular and cellular mechanisms by which CD4+CD25+ T cells a re induced and the mechanism by which they inhibit induction of autoimmunity is crucial and has not yet been elucidated.Recently, the expression of the transcription Foxp3 factor was shown to be enriched in CD4+CD25+ Treg cells and forced expression of Foxp3 was shown to convert murine naïve T cells into regulatory T cells. Foxp3 may initiate a genetic program that converts naïve T cells into anergic cells, which then function as Tregs.In this work, we propose to study the central role of Foxp3 in inhibiting effector functions, inducing anergy, and generating regulatory T cells in vivo. This work will permit me to study the molecular mechanisms of tolerance.
Оригинален текст от CORDIS (на английски).
Участници
- UNIVERSITé PIERRE ET MARIE CURIE - PARIS 6 · PARISКоординаторНиво градФранция
- BRIGHAM AND WOMEN HARVARD MEDICAL SCHOOL · BOSTON MAНиво градСъединени щати
Връзки
Данни: CORDIS, © Европейски съюз