Autophagy gene Atg16L1 prevents lethal T cell alloreactivity mediated by dendritic cells.
Immunity
; 41(4): 579-91, 2014 Oct 16.
Article
en En
| MEDLINE
| ID: mdl-25308334
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.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Células Dendríticas
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Linfocitos T CD4-Positivos
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Proteínas Portadoras
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Linfocitos T CD8-positivos
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Enfermedad Injerto contra Huésped
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Immunity
Asunto de la revista:
ALERGIA E IMUNOLOGIA
Año:
2014
Tipo del documento:
Article
País de afiliación:
Estados Unidos