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Lookup NU author(s): Professor Anne Dickinson
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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.
Author(s): Hubbard-Lucey VM, Shono Y, Maurer K, West ML, Singer NV, Ziegler CGK, Lezcano C, Motta ACF, Schmid K, Levi SM, Murphy GF, Liu C, Winkler JD, Amaravadi RK, Rogler G, Dickinson AM, Holler E, van den Brink MRM, Cadwell K
Publication type: Article
Publication status: Published
Journal: Immunity
Year: 2014
Volume: 41
Issue: 4
Pages: 579-591
Print publication date: 16/10/2014
Online publication date: 09/10/2014
Acceptance date: 13/09/2014
ISSN (print): 1074-7613
ISSN (electronic): 1097-4180
Publisher: Cell Press
URL: http://dx.doi.org/10.1016/j.immuni.2014.09.011
DOI: 10.1016/j.immuni.2014.09.011
PubMed id: 25308334
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