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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| Fformat: | Traethawd Ymchwil |
| Iaith: | English |
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2021
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| Crynodeb: | <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> |
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