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Updated: Apr 22, 2026

Generation of Human Alloantigen-specific T Cells from Peripheral Blood
Published on: November 21, 2014
Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells
Vanessa M Hubbard-Lucey1, Yusuke Shono2, Katie Maurer3
1Kimmel Center for Biology and Medicine at the Skirball Institute, New York, NY 10016, USA; Department of Microbiology, New York University School of Medicine, New York, NY 10016, USA.
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.
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