| First Author | Hubbard-Lucey VM | Year | 2014 |
| Journal | Immunity | Volume | 41 |
| Issue | 4 | Pages | 579-91 |
| PubMed ID | 25308334 | Mgi Jnum | J:250095 |
| Mgi Id | MGI:6101703 | Doi | 10.1016/j.immuni.2014.09.011 |
| Citation | Hubbard-Lucey VM, et al. (2014) Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells. Immunity 41(4):579-91 |
| abstractText | Atg16L1 mediates the cellular degradative process of autophagy and is considered a critical regulator of inflammation based on its genetic association with inflammatory bowel disease. Here we find that Atg16L1 deficiency leads to an exacerbated graft-versus-host disease (GVHD) in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Atg16L1-deficient allo-HSCT recipients with GVHD displayed increased T cell proliferation due to increased dendritic cell (DC) numbers and costimulatory molecule expression. Reduced autophagy within DCs was associated with lysosomal abnormalities and decreased amounts of A20, a negative regulator of DC activation. These results broaden the function of Atg16L1 and the autophagy pathway to include a role in limiting a DC-mediated response during inflammatory disease, such as GVHD. |
