AE-CCL18 · CCL18 - a susceptibility gene for atopic eczema regulated by host-microbe interactions?
6РП — Действия „Мария Кюри“
- Период
- 2007-01-01 → 2008-12-31
- Финансиране от ЕС
- 166 488 €
- Участници
- 1
- Схема
- EIF
Линиите свързват координатора с партньорите.
Накратко на български
МикроРНК-тата в кожата на хора с атопичен екзема се анализират, като се проследява например нивото на miR-155. Това помага да се разбере как се регулира имунният отговор и кои молекули могат да бъдат мишени за бъдещо лечение.
Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.
Резултати накратко
Final Activity Report Summary - AE-CCL18 (CCL18 - a susceptibility gene for atopic eczema regulated by host-microbe interactions?)
The goal of our project was to explore the possibility that deregulated expression of a new family of genes, microRNAs (miRNAs), plays a role in atopic skin inflammation. The expression or function of microRNAs had not been described in human skin or in atopic eczema before our investigation. There were several major achievements from this project. First, we demonstrated the deregulated expression of miRNAs in atopic eczema skin in comparison to healthy skin (Sonkoly et al., 2007). Our results demonstrate that lesional skin of atopic eczema patients is characterised by a specific, non-random miRNA expression profile that differs from that of healthy skin or another type of chronic skin inflammation, psoriasis (Sonkoly et al., 2007). Second, we identified miR-155 as a miRNA that may be a potential therapeutic target for the treatment of atopic eczema in the future (unpublished data). miR-155 levels are significantly higher in inflamed atopic eczea skin than in healthy skin. miR-155 is expressed by T lymphocytes, cells that play a central role in inflammation. We demonstrated that miR-155 regulates the proliferation of T lymphocytes, therefore it has important role in the regulation of the immune response.
Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз
Цел на проекта
Atopic disorders are a group of increasingly common multifactorial chronic diseases, which cause inflammatory and degenerative changes in the skin and mucosal surfaces. Among those diseases, atopic eczema represents the most prevalent condition affecting u p to 22% of the paediatric and 1-3% of adult population.The aetiology of atopic eczema involves environmental, genetic and immunological factors. For the prevention and treatment of this disease, advances are needed in the identification of susceptibility factors, disease markers and therapeutic targets. The skin-specific trafficking of inflammatory cells during atopic eczema is regulated by chemokines. CCL18 is the most highly and specifically expressed chemokine in atopic eczema.We will analyze the role of single nucleotide polymorphisms in the CCL18 gene in the susceptibility for atopic eczema using an exceptional size of DNA sample collection (n = 3111) obtained from atopic and non-atopic individuals. Furthermore, we will analyze the methylation status of CCL18 gene in atopic eczema patients in comparison to healthy controls.Additionally, we will examine whether the serum level of CCL18 correlates with disease severity, therapeutic treatments and trigger factors, using large number of well-characterize d samples obtained from atopic eczema patients and healthy individuals. The host's previous work demonstrated an important role for the opportunistic yeast Malassezia in triggering the IgE- and T cell-mediated inflammation in atopic eczema patients.Hence, we will investigate whether Malassezia allergens can be responsible for the elevated level of CCL18 in atopic lesional skin by examining CCL18 expression in all relevant structural cells of the skin as well as in dendritic cells and mast cells.This project aims to increase our knowledge about susceptibility factors, disease markers and the pathogenesis of atopic eczema, which may contribute to prospective prevention studies and new treatment strategies.
Оригинален текст от CORDIS (на английски).
Участници
- KAROLINSKA INSTITUTET · STOCKHOLMКоординаторШвеция
Връзки
Данни: CORDIS, © Европейски съюз