The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products

We identified a critical role for receptor for advanced glycation end products (RAGE) in the intratumoral accumulation of myeloid-derived suppressor cells (MDSCs) during pancreatic carcinogenesis. The absence of RAGE markedly delayed neoplasia and limited MDSC accumulation in mice expressing an onco...

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Detalles Bibliográficos
Autores principales: Vernon, Philip J., Zeh III, Herbert J., Lotze, Michael T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667906/
https://www.ncbi.nlm.nih.gov/pubmed/23762800
http://dx.doi.org/10.4161/onci.24184
Descripción
Sumario:We identified a critical role for receptor for advanced glycation end products (RAGE) in the intratumoral accumulation of myeloid-derived suppressor cells (MDSCs) during pancreatic carcinogenesis. The absence of RAGE markedly delayed neoplasia and limited MDSC accumulation in mice expressing an oncogenic variant of Kras. In spite of MDSCs, these mice accumulated non-immunosuppressive macrophages. Thus, RAGE regulates carcinogenesis and consequent myeloid responses.

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