Identification of a rat bone marrow-derived dendritic cell population which secretes both IL-10 and IL-12: Evidence against a reciprocal relationship between IL-10 and IL-12 secretion

Muthana, Munitta; Fairburn, Barbara; Mirza, Shabana; Slack, Laura K.; Hopkinson, Kay; Pockley, A. Graham

doi:10.1016/j.imbio.2006.02.001

Cited by 13 publications

(12 citation statements)

References 73 publications

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“…As we have reported previously, no fluorescent staining of this population of immature rat BMDCs [59,60] is observed when incubations are performed at 4°C, whereas cells do become positive when incubations are performed at 37°C (Fig. 2).…”

supporting

confidence: 80%

“…We have previously reported a strategy for generating a population of immature rat bone marrow-derived DCs (BMDCs) [59,60], and demonstrated that these do not express cell surface receptors for gp96 [56]. However, these cells do internalize gp96 via non receptor-mediated endocytosis in the absence of any overt effect on their phenotype [56].…”

Section: Introductionmentioning

confidence: 99%

“…This approach induces the differentiation of large numbers of a homogeneous population of adherent cells (typically 1.2×10 6 adherent cells/flask), all of which exhibit the morphological appearance of DCs and 90% of which stain positive with the OX62 mAb [59]. The purity of each population can be confirmed by multicolor flow cytometry thus:…”

mentioning

confidence: 99%

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A non-receptor-mediated mechanism for internalization of molecular chaperones

Pockley

Fairburn

Mirza

et al. 2007

Methods

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The evolving realization that stress proteins, which have for many years been considered to be exclusively intracellular molecules under normal conditions, can be released from viable cells via a number of potential routes/pathways has prompted interest into their extracellular biology and intercellular signaling properties. That the stress proteins Hsp60, Hsp70 and gp96 can elicit both proand anti-inflammatory effects suggests that these molecules play a key role in the maintenance of immunological homeostasis, and a better understanding of the immunobiology of extracellular stress proteins might reveal new and more effective approaches for controlling and managing infectious disease, inflammatory disease and cancer. A number of cell surface receptors for stress proteins have been identified, and the intracellular consequences of these cell surface receptor-ligand interactions have been characterized. To date, studies into the intercellular signaling properties of stress proteins and their interactions with antigen presenting cells have focused on specific receptor-mediated uptake, and have not considered the fact that such cells can also take up proteins via non-specific endocytosis/pinocytosis. Herein we present a methodological approach for assessing receptormediated and non-receptor mediated uptake of gp96 by rat bone marrow-derived dendritic cells.

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supporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

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A non-receptor-mediated mechanism for internalization of molecular chaperones

Pockley

Fairburn

Mirza

et al. 2007

Methods

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“…The other possible effect is that the redirection of iDC differentiation might reduce the number of functional DCs, limiting the potential antitumor immune effect. In fact, many studies have shown that tumor patients have defects in DC maturation, and the number of functional DCs is reduced, which leads to immune suppression (31,32).…”

Section: Discussionmentioning

confidence: 99%

VEGF-A not Ang2 mediates endothelial-like differentiation of immature DCs by ERK1/2 signaling in the microenvironment of human colon adenocarcinoma

Lü

Liu²,

Zhao³

et al. 2011

Int J Oncol

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Abstract. Endothelial-like differentiation of dendritic cells (DCs) is an interesting and significant phenomenon, which is worth further investigation. Here, we show that the tumor microenvironment derived from the supernatant of the SW620 human colon adenocarcinoma cell line and colon adenocarcinoma tissue homogenate can promote immature DCs (iDCs) to differentiate from the DC pathway toward endothelial cells, while the peri-carcinoma homogenate supernatant does not have this role. Inhibition of angiopoietin-2 (Ang2) in the supernatant by its antibody has no obvious influence on the endotheliallike differentiation. In contrast, inhibition of vascular endothelial growth factor-A (VEGF-A) blocked the differentiation. During the course of differentiation, a sustained activation of ERK1/2 was detected. PD98059 blocked the phosphorylation of ERK1/2 as well as the endothelial-like differentiation of iDCs. Inhibition of VEGF-A also blocked the phosphorylation of ERK1/2. These data suggest that VEGF-A not Ang2 mediates endothelial-like differentiation of iDCs by ERK1/2 signaling in the microenvironment of human colon adenocarcinoma.

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“…This approach induces the differentiation of large numbers of a homogeneous population of adherent cells (typically 1.2 ϫ 10 6 adherent cells/flask), all of which exhibit the morphological appearance of DCs and Ͼ90% of which bind the OX62 monoclonal antibody (mAb; Muthana et al 2006). The OX62 mAb recognizes the 150-kDa integrin ␣ E2 subunit and was originally described as being expressed on most, if not all, DCs in the rat (Brenan and Puklavec 1992).…”

Section: Generation Of Rat Bmdcsmentioning

confidence: 99%

The stress protein gp96 is not an activator of resting rat bone marrow–derived dendritic cells, but is a costimulator and activator of CD3+ T cells

Mirza¹,

Muthana²,

Fairburn³

et al. 2006

Cell Stress Chaper

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Although low doses of tumor-derived stress protein gp96 elicit protective immunity to the tumor from which it is isolated, protection is lost at high doses because of the induction of immunoregulatory CD4 ϩ T cells. This study evaluated the influence of gp96 on resting rat bone marrow-derived dendritic cells (BMDCs) and purified CD3 ϩ T cells. In contrast to previous reports, gp96 had no effect on adhesion and costimulatory molecule expression by BMDCs, nor did it influence interleukin (IL)-10 and IL-12 secretion or their allostimulatory capacity. Gp96 did not bind to BMDCs but dose-dependently bound to CD4 ϩ and CD8 ϩ T cells. At low concentrations (1 and 25 g/mL), gp96 acted as a costimulator of CD3 ϩ T cells, inducing proliferation and the secretion of interferon (IFN)-␥ and IL-10. Gp96 also increased the proliferation of CD28-costimulated CD3 ϩ T cells and their secretion of IFN-␥, IL-4, and IL-10. Gp96 had no effect at higher concentrations (50 and 100 g/mL), despite the occurrence of cell surface binding at these concentrations. These findings indicate that gp96 can act as a costimulatory molecule for CD3 ϩ T cells, and an observed increase in the IL-10:IFN-␥ secretion ratio induced by gp96 suggests that it might, at appropriate concentrations, promote a regulatory T-helper 2 (Th2)-like phenotype.

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Identification of a rat bone marrow-derived dendritic cell population which secretes both IL-10 and IL-12: Evidence against a reciprocal relationship between IL-10 and IL-12 secretion

Cited by 13 publications

References 73 publications

A non-receptor-mediated mechanism for internalization of molecular chaperones

A non-receptor-mediated mechanism for internalization of molecular chaperones

VEGF-A not Ang2 mediates endothelial-like differentiation of immature DCs by ERK1/2 signaling in the microenvironment of human colon adenocarcinoma

The stress protein gp96 is not an activator of resting rat bone marrow–derived dendritic cells, but is a costimulator and activator of CD3+ T cells

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