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Federal government websites often end in. The site is secure. Preview improvements coming to the PMC website in October Learn More or Try it out now. A polymorphism in the autophagy gene Atg16l1 is associated with susceptibility to inflammatory bowel disease IBD ; however, it remains unclear how autophagy contributes to intestinal immune homeostasis.
Moreover, we also identify an unexpected role for autophagy in directly limiting mucosal T H 2 cell expansion. These findings provide new insights into the reciprocal control of distinct intestinal T H cell responses by autophagy, with important implications for understanding and treatment of chronic inflammatory disorders. The gut presents a puzzle to our immune system. Immune cells must rapidly respond to antigens produced by harmful bacteria, but food and the beneficial bacteria that inhabit the gut also produce antigens that our immune system must tolerate.
Inappropriate immune responses in the gut can lead to inflammatory bowel disease, a debilitating disease with no current cure. We do not fully understand why these harmful inflammatory responses arise, but we know that genetic factors are important. Mutations in genes that affect a process known as autophagy — a pathway that breaks down and recycles unwanted material inside cells — make inflammatory bowel disease more likely to develop, but exactly how they do so remains unclear.
T helper cells are crucial controllers of intestinal immune responses and changes in their numbers and behaviour occur during inflammatory bowel disease. Kabat et al. Blocking autophagy in T cells altered the balance of different types of T helper cells in the gut. A crucial population of regulatory T cells, which keep inflammatory responses in check, was lost.