Human myeloid dendritic cells treated with supernatants of rotavirus infected Caco-2 cells induce a poor Th1 response

We have previously shown that human myeloid dendritic cells treated with purified rotavirus induce an allogenic Th1 response. To determine if rotavirus in the context of an intestinal microenvironment modulates the function of dendritic cells, we treated these cells with supernatants from non-infect...

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Autores:
Tipo de recurso:
Fecha de publicación:
2012
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/23645
Acceso en línea:
https://doi.org/10.1016/j.cellimm.2011.10.017
https://repository.urosario.edu.co/handle/10336/23645
Palabra clave:
Thymic stromal lymphopoietin
Transforming growth factor beta1
Article
Cell strain caco 2
Cellular immunity
Controlled study
Cytokine production
Human
Human cell
Immunomodulation
Intestine mucosa
Myeloid dendritic cell
Priority journal
Rotavirus infection
Supernatant
Th1 cell
Th2 cell
Virus neutralization
Caco-2 cells
Cd4-positive t-lymphocytes
Cellular microenvironment
Coculture techniques
Cytokines
Dendritic cells
Hla-dr antigens
Humans
Immunologic factors
Myeloid cells
Rotavirus
Rotavirus infections
Th1 cells
Th2 cells
Transforming growth factor beta1
Rotavirus
Caco-2 cells
Dendritic cells
Immunomodulators
Rotavirus
Tgf-?1
cd86
messenger
cultured
Antigens
Rna
Tumor cells
Rights
License
Abierto (Texto Completo)
Description
Summary:We have previously shown that human myeloid dendritic cells treated with purified rotavirus induce an allogenic Th1 response. To determine if rotavirus in the context of an intestinal microenvironment modulates the function of dendritic cells, we treated these cells with supernatants from non-infected or infected Caco-2 cells and studied their capacity to promote Th1 or Th2 responses. Dendritic cells treated with supernatants from rotavirus-infected Caco-2 cells promoted a significantly lower Th1 response, in comparison with those treated with purified rotavirus. We wanted to establish if TGF-?1, induced, or TSLP, not induced, during rotavirus infection, could mediate this effect. Neutralization of TGF-? but not TSLP in the supernatant prior to treatment of dendritic cells increased their capacity to promote a Th1 response. The results suggest that the TGF-?1 induced by rotavirus could be an immune evasion mechanism, and may partially explain the poor rotavirus-specific T cell response we have previously evidenced. © 2011 Elsevier Inc.