Regulation of intestinal T cell homeostasis by autophagy
<p>Mice in which the autophagy protein ATG16L1 was selectively ablated in T cells develop spontaneous intestinal inflammation, characterized by loss of Foxp3+ Treg cells and a selective expansion of Gata3+ Th2 cells. This phenotype was most pronounced in the colonic lamina propria. Thus, a lac...
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| Formato: | Thesis |
| Idioma: | English |
| Publicado em: |
2021
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| _version_ | 1826315879383564288 |
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| author | Dumitru, C |
| author2 | Maloy, K |
| author_facet | Maloy, K Dumitru, C |
| author_sort | Dumitru, C |
| collection | OXFORD |
| description | <p>Mice in which the autophagy protein ATG16L1 was selectively ablated in T cells develop spontaneous intestinal inflammation, characterized by loss of Foxp3+ Treg cells and a selective expansion of Gata3+ Th2 cells. This phenotype was most pronounced in the colonic lamina propria. Thus, a lack of autophagy simultaneously reduces anti-inflammatory Treg cells and increases pro-inflammatory Th2 effector cells in the intestine. This discrepancy could be partly attributed to an altered metabolic programme employed by Atg16l1-deficient Treg cells, with increased glycolysis and impaired fatty acid metabolism. In contrast, the metabolic profile of in vitro polarized Th2 cells seemed to be independent of autophagy. </p>
<p>The aims of this thesis are to investigate the mechanistic consequences of altered autophagy in different T cell subsets and also to explore the link between the dominant type 2 immune responses and the observed intestinal pathology.</p> |
| first_indexed | 2024-03-06T19:40:50Z |
| format | Thesis |
| id | oxford-uuid:209e8a35-a833-48f3-a7fd-132eb57a9cfe |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-12-09T03:34:13Z |
| publishDate | 2021 |
| record_format | dspace |
| spelling | oxford-uuid:209e8a35-a833-48f3-a7fd-132eb57a9cfe2024-12-01T17:46:11ZRegulation of intestinal T cell homeostasis by autophagyThesishttp://purl.org/coar/resource_type/c_db06uuid:209e8a35-a833-48f3-a7fd-132eb57a9cfeImmunologypathologymolecular biologyEnglishHyrax Deposit2021Dumitru, CMaloy, KSimon, A<p>Mice in which the autophagy protein ATG16L1 was selectively ablated in T cells develop spontaneous intestinal inflammation, characterized by loss of Foxp3+ Treg cells and a selective expansion of Gata3+ Th2 cells. This phenotype was most pronounced in the colonic lamina propria. Thus, a lack of autophagy simultaneously reduces anti-inflammatory Treg cells and increases pro-inflammatory Th2 effector cells in the intestine. This discrepancy could be partly attributed to an altered metabolic programme employed by Atg16l1-deficient Treg cells, with increased glycolysis and impaired fatty acid metabolism. In contrast, the metabolic profile of in vitro polarized Th2 cells seemed to be independent of autophagy. </p> <p>The aims of this thesis are to investigate the mechanistic consequences of altered autophagy in different T cell subsets and also to explore the link between the dominant type 2 immune responses and the observed intestinal pathology.</p> |
| spellingShingle | Immunology pathology molecular biology Dumitru, C Regulation of intestinal T cell homeostasis by autophagy |
| title | Regulation of intestinal T cell homeostasis by autophagy |
| title_full | Regulation of intestinal T cell homeostasis by autophagy |
| title_fullStr | Regulation of intestinal T cell homeostasis by autophagy |
| title_full_unstemmed | Regulation of intestinal T cell homeostasis by autophagy |
| title_short | Regulation of intestinal T cell homeostasis by autophagy |
| title_sort | regulation of intestinal t cell homeostasis by autophagy |
| topic | Immunology pathology molecular biology |
| work_keys_str_mv | AT dumitruc regulationofintestinaltcellhomeostasisbyautophagy |