Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8alpha+ dendritic cells

Despite lack of tumor control in many models, spontaneous T cell priming occurs frequently in response to a growing tumor. However, the innate immune mechanisms that promote natural antitumor T cell responses are undefined. In human metastatic melanoma, there was a correlation between a type I inter...

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Detalles Bibliográficos
Autores: Fuertes, Mercedes Beatriz, Kacha, Aalok K., Kline, Justin, Woo, Seng Ryong, Kranz, David M., Murphy, Kenneth M., Gajewski, Thomas F.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2011
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/10886
Acceso en línea:http://hdl.handle.net/11336/10886
Access Level:acceso abierto
Palabra clave:INTERFERON
TUMOR
CD8 T CELL
DENDRITIC CELL
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:Despite lack of tumor control in many models, spontaneous T cell priming occurs frequently in response to a growing tumor. However, the innate immune mechanisms that promote natural antitumor T cell responses are undefined. In human metastatic melanoma, there was a correlation between a type I interferon (IFN) transcriptional profile and T cell markers in metastatic tumor tissue. In mice, IFN-b was produced by CD11c(+) cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacking IFN-a/bR or Stat1. IFN signaling was required in the hematopoietic compartment at the level of host antigen-presenting cells, and selectively for intratumoral accumulation of CD8a(+) dendritic cells, which were demonstrated to be essential using Batf3(-/-) mice. Thus, host type I IFNs are critical for the innate immune recognition of a growing tumor through signaling on CD8alfa(+) DCs.