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DNGR-1 en las células dendríticas limita el daño tisular al amortiguar el reclutamiento de neutrófilos
Carlos Del Fresno1, Paula Saz-Leal2, Michel Enamorado2
1Immunobiology Laboratory, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. dsancho@cnic.es cdelfresno@cnic.es.
Science (New York, N.Y.)
|October 20, 2018
Resumen
El receptor del grupo de lectinas asesinas naturales de células dendríticas-1 (DNGR-1) limita las respuestas inflamatorias y el daño tisular después de la lesión. La deficiencia de DNGR-1 exacerba la pancreatitis y la patología infecciosa al aumentar la neutrofilia.
Área de la Ciencia:
- Inmunología
- Biología celular
- Enfermedades infecciosas
Sus antecedentes:
- La lesión del huésped activa los mecanismos de retroalimentación para limitar el daño tisular.
- Las células dendríticas convencionales de tipo 1 (cDC1s) expresan DNGR-1 (codificado por Clec9a), detectando el daño tisular y promoviendo la presentación cruzada a las células T CD8+.
Objetivo del estudio:
- Investigar el papel de DNGR-1 en la regulación de las respuestas inflamatorias a la lesión de tejidos estériles e infecciosos.
- Para aclarar los mecanismos por los cuales DNGR-1 influye en la inflamación dañina del huésped.
Principales métodos:
- Se utilizaron modelos de ratón de lesión estéril (pancreatitis inducida por la caeruleína) y lesión infecciosa (infección sistémica por Candida albicans).
- Patología evaluada, infiltración de células inmunes (neutrofilia) y producción de citoquinas (MIP-2/Cxcl2) en ratones de tipo salvaje y con deficiencia de DNGR-1.
- Investigó la participación de la vía de señalización SHP-1.
Principales resultados:
- La deficiencia de DNGR-1 exacerbó la pancreatitis necrotizante y la patología de la infección por Candida albicans.
- Se observó un aumento de la neutrofilia en ratones con deficiencia de DNGR-1, independientemente de las células B y T.
- El compromiso de DNGR- 1 activó a SHP- 1 e inhibió la producción de MIP- 2 por parte de los cDC1 durante la infección por Candida, restringiendo el reclutamiento de neutrófilos.
Conclusiones:
- DNGR-1 actúa como un regulador crítico de las respuestas inmunes innatas y el daño tisular.
- La señalización DNGR-1 en cDC1s restringe el reclutamiento de neutrófilos y promueve la tolerancia a la enfermedad, controlando así la inmunopatología.
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