Hubbard-Lucey, Vanessa M. and Shono, Yusuke and Maurer, Katie and West, Mallory L. and Singer, Natalie V. and Ziegler, Carly G. K. and Lezcano, Cecilia and Motta, Ana Carolina Fragoso and Schmid, Karin and Levi, Samuel M. and Murphy, George F. and Liu, Chen and Winkler, Jeffrey D. and Amaravadi, Ravi K. and Rogler, Gerhard and Dickinson, Anne M. and Holler, Ernst and van den Brink, Marcel R. M. and Cadwell, Ken (2014) Autophagy Gene Atg16l1 Prevents Lethal T Cell Alloreactivity Mediated by Dendritic Cells. IMMUNITY, 41 (4). pp. 579-591. ISSN 1074-7613, 1097-4180
Full text not available from this repository. (Request a copy)Abstract
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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | VERSUS-HOST-DISEASE; TRANSMEMBRANE 5; STEM-CELL; PROTEIN; EXPRESSION; DEGRADATION; LAPTM5; TRANSPLANTATION; MECHANISMS; PHAGOSOMES; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin III (Hämatologie und Internistische Onkologie) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 08 Aug 2019 12:38 |
| Last Modified: | 08 Aug 2019 12:38 |
| URI: | https://pred.uni-regensburg.de/id/eprint/9346 |
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