Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells.
Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naïve CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). In this study, we have analysed whether the specialised features of CD103(+) DC are conserved in colitis. Our results sh...
| Главные авторы: | , , |
|---|---|
| Формат: | Journal article |
| Язык: | English |
| Опубликовано: |
2010
|
| _version_ | 1826295487142035456 |
|---|---|
| author | Laffont, S Siddiqui, K Powrie, F |
| author_facet | Laffont, S Siddiqui, K Powrie, F |
| author_sort | Laffont, S |
| collection | OXFORD |
| description | Intestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naïve CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). In this study, we have analysed whether the specialised features of CD103(+) DC are conserved in colitis. Our results show that inflammation dampens the tolerogenic properties of MLN CD103(+) DC, which is associated with lower expression of tgfbeta2 and aldh1a2. Accordingly, CD103(+) DC taken from colitic mice are impaired in their ability to induce Foxp3(+) Treg and instead favour the emergence of IFN-gamma-producing CD4(+) T cells compared with their steady-state counterparts. BrdU-labelling studies and analysis of ontogeny markers show that CD103(+) DC from steady-state and colitic settings retain similar subset composition and developmental pathways. These results indicate that MLN CD103(+) DC are not hard-wired to promote tolerance but can adapt to environmental conditions. The inflammatory properties of MLN CD103(+) DC in colitic mice may reflect defective gut tolerogenic conditioning or altered migratory pathways and raise the possibility that migratory DC populations contribute to the pathogenesis of inflammatory bowel disease. |
| first_indexed | 2024-03-07T04:01:47Z |
| format | Journal article |
| id | oxford-uuid:c4d12a54-fbd7-4b64-91be-b1d9a8db998b |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T04:01:47Z |
| publishDate | 2010 |
| record_format | dspace |
| spelling | oxford-uuid:c4d12a54-fbd7-4b64-91be-b1d9a8db998b2022-03-27T06:26:27ZIntestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:c4d12a54-fbd7-4b64-91be-b1d9a8db998bEnglishSymplectic Elements at Oxford2010Laffont, SSiddiqui, KPowrie, FIntestinal CD103(+) DC promote the differentiation of Foxp3(+) Treg from naïve CD4(+) T cells through mechanisms involving TGF-beta and the dietary metabolite, retinoic acid (RA). In this study, we have analysed whether the specialised features of CD103(+) DC are conserved in colitis. Our results show that inflammation dampens the tolerogenic properties of MLN CD103(+) DC, which is associated with lower expression of tgfbeta2 and aldh1a2. Accordingly, CD103(+) DC taken from colitic mice are impaired in their ability to induce Foxp3(+) Treg and instead favour the emergence of IFN-gamma-producing CD4(+) T cells compared with their steady-state counterparts. BrdU-labelling studies and analysis of ontogeny markers show that CD103(+) DC from steady-state and colitic settings retain similar subset composition and developmental pathways. These results indicate that MLN CD103(+) DC are not hard-wired to promote tolerance but can adapt to environmental conditions. The inflammatory properties of MLN CD103(+) DC in colitic mice may reflect defective gut tolerogenic conditioning or altered migratory pathways and raise the possibility that migratory DC populations contribute to the pathogenesis of inflammatory bowel disease. |
| spellingShingle | Laffont, S Siddiqui, K Powrie, F Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title | Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title_full | Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title_fullStr | Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title_full_unstemmed | Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title_short | Intestinal inflammation abrogates the tolerogenic properties of MLN CD103+ dendritic cells. |
| title_sort | intestinal inflammation abrogates the tolerogenic properties of mln cd103 dendritic cells |
| work_keys_str_mv | AT laffonts intestinalinflammationabrogatesthetolerogenicpropertiesofmlncd103dendriticcells AT siddiquik intestinalinflammationabrogatesthetolerogenicpropertiesofmlncd103dendriticcells AT powrief intestinalinflammationabrogatesthetolerogenicpropertiesofmlncd103dendriticcells |