| First Author | Plaza-Sirvent C | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 705436 | PubMed ID | 34512629 |
| Mgi Jnum | J:312741 | Mgi Id | MGI:6765886 |
| Doi | 10.3389/fimmu.2021.705436 | Citation | Plaza-Sirvent C, et al. (2021) A Central Role for Atg5 in Microbiota-Dependent Foxp3(+) RORgammat(+) Treg Cell Preservation to Maintain Intestinal Immune Homeostasis. Front Immunol 12:705436 |
| abstractText | Autophagy is an evolutionary conserved catabolic pathway that ensures the degradation of intracellular components. The autophagic pathway is regulated by autophagy-related (Atg) proteins that govern formation of double-membraned vesicles called autophagosomes. Autophagy deficiency in regulatory T (Treg) cells leads to increased apoptosis of these cells and to the development of autoimmune disorders, predominantly characterized by intestinal inflammation. Recently, RORgammat-expressing Treg cells have been identified as key regulators of gut homeostasis, preventing intestinal immunopathology. To study the role of autophagy in RORgammat(+) Foxp3(+) Treg cells, we generated mice lacking the essential component of the core autophagy machinery Atg5 in Foxp3(+) cells. Atg5 deficiency in Treg cells led to a predominant intestinal inflammation. While Atg5-deficient Treg cells were reduced in peripheral lymphoid organs, the intestinal RORgammat(+) Foxp3(+) subpopulation of Treg cells was most severely affected. Our data indicated that autophagy is essential to maintain the intestinal RORgammat(+) Foxp3(+) Treg population, thereby protecting the mice from gut inflammatory disorders. |
