Silencing of the glucocorticoid-induced leucine zipper improves the immunogenicity of clinical-grade dendritic cells

Dominique Cathelin; Özcan Met; Inge Marie Svane

doi:10.1016/j.jcyt.2013.02.005

Silencing of the glucocorticoid-induced leucine zipper improves the immunogenicity of clinical-grade dendritic cells

Dominique Cathelin, Özcan Met, Inge Marie Svane

14 Citationer (Scopus)

Abstract

The maturation cocktail composed of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and prostaglandin E2 is considered the "gold standard" for inducing the maturation of dendritic cells (DCs) for use in cancer immunotherapy. Nevertheless, although this maturation cocktail induces increased expression of several activation markers, such as CD83, the co-stimulation molecules CD80, CD86 and CD40 and the chemokine receptor involved in DC homing in lymph nodes CCR7, the DC immune stimulatory function in vivo contrasts with this mature phenotype, and good clinical outcomes in patients with cancer treated with DC-based vaccines remain rare.

Originalsprog	Engelsk
Tidsskrift	Cytotherapy
Vol/bind	15
Udgave nummer	6
Sider (fra-til)	740-9
Antal sider	10
ISSN	1465-3249
DOI	https://doi.org/10.1016/j.jcyt.2013.02.005
Status	Udgivet - jun. 2013

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10.1016/j.jcyt.2013.02.005

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title = "Silencing of the glucocorticoid-induced leucine zipper improves the immunogenicity of clinical-grade dendritic cells",

abstract = "The maturation cocktail composed of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and prostaglandin E2 is considered the {"}gold standard{"} for inducing the maturation of dendritic cells (DCs) for use in cancer immunotherapy. Nevertheless, although this maturation cocktail induces increased expression of several activation markers, such as CD83, the co-stimulation molecules CD80, CD86 and CD40 and the chemokine receptor involved in DC homing in lymph nodes CCR7, the DC immune stimulatory function in vivo contrasts with this mature phenotype, and good clinical outcomes in patients with cancer treated with DC-based vaccines remain rare.",

author = "Dominique Cathelin and {\"O}zcan Met and Svane, {Inge Marie}",

year = "2013",

month = jun,

doi = "10.1016/j.jcyt.2013.02.005",

language = "English",

volume = "15",

pages = "740--9",

journal = "Cytotherapy",

issn = "1465-3249",

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TY - JOUR

T1 - Silencing of the glucocorticoid-induced leucine zipper improves the immunogenicity of clinical-grade dendritic cells

AU - Cathelin, Dominique

AU - Met, Özcan

AU - Svane, Inge Marie

PY - 2013/6

Y1 - 2013/6

N2 - The maturation cocktail composed of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and prostaglandin E2 is considered the "gold standard" for inducing the maturation of dendritic cells (DCs) for use in cancer immunotherapy. Nevertheless, although this maturation cocktail induces increased expression of several activation markers, such as CD83, the co-stimulation molecules CD80, CD86 and CD40 and the chemokine receptor involved in DC homing in lymph nodes CCR7, the DC immune stimulatory function in vivo contrasts with this mature phenotype, and good clinical outcomes in patients with cancer treated with DC-based vaccines remain rare.

AB - The maturation cocktail composed of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and prostaglandin E2 is considered the "gold standard" for inducing the maturation of dendritic cells (DCs) for use in cancer immunotherapy. Nevertheless, although this maturation cocktail induces increased expression of several activation markers, such as CD83, the co-stimulation molecules CD80, CD86 and CD40 and the chemokine receptor involved in DC homing in lymph nodes CCR7, the DC immune stimulatory function in vivo contrasts with this mature phenotype, and good clinical outcomes in patients with cancer treated with DC-based vaccines remain rare.

U2 - 10.1016/j.jcyt.2013.02.005

DO - 10.1016/j.jcyt.2013.02.005

M3 - Journal article

C2 - 23643305

SN - 1465-3249

VL - 15

SP - 740

EP - 749

JO - Cytotherapy

JF - Cytotherapy

IS - 6

ER -

Silencing of the glucocorticoid-induced leucine zipper improves the immunogenicity of clinical-grade dendritic cells

Abstract

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