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Collagen I enhances functional activities of human monocyte-derived dendritic cells via discoidin domain receptor 2.
Poudel, Barun; Yoon, Dong-Sik; Lee, Jeong-Heon; Lee, Young-Mi; Kim, Dae-Ki.
Afiliación
  • Poudel B; Department of Immunolgy and Institute of Medical Sciences, Chonbuk National University Medical School, Jeonju, Jeonbuk 561-756, Republic of Korea.
Cell Immunol ; 278(1-2): 95-102, 2012.
Article en En | MEDLINE | ID: mdl-23121981
We evaluated the involvement of collagen and their discoidin domain receptors (DDRs), DDR1 and DDR2, on the activation of human monocyte-derived dendritic cells (hDCs). DDR2 was markedly expressed on mature hDCs in comparison to immature ones. Collagen I enhanced the release of IL-12p40, TNF-α and IFN-γ by hDCs. Additionally, hDCs exhibited enhanced expression of costimulatory molecules, and potent functional activities which, in turn, has therapeutic value. Interestingly, DDR2 depletion showed decrease in capacity of hDCs to stimulate T cells proliferation, whereas DDR1 silencing had no significant affect. These data demonstrate that DDR2 enhances hDCs activation and contributes to their functional activities. In addition, application of collagen I treated dendritic cells (DCs) vaccine reduced tumor burden giving longer survival in melanoma mice. Our study suggests that collagen I may enhance functional activities of DCs in immune response.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Contexto en salud: 1_ASSA2030 Problema de salud: 1_doencas_nao_transmissiveis Asunto principal: Células Dendríticas / Receptores Mitogénicos / Proteínas Tirosina Quinasas Receptoras / Colágeno Tipo I Idioma: En Revista: Cell Immunol Año: 2012 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Contexto en salud: 1_ASSA2030 Problema de salud: 1_doencas_nao_transmissiveis Asunto principal: Células Dendríticas / Receptores Mitogénicos / Proteínas Tirosina Quinasas Receptoras / Colágeno Tipo I Idioma: En Revista: Cell Immunol Año: 2012 Tipo del documento: Article
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