Presentation of donor major histocompatibility complex antigens by bone marrow dendritic cell-derived exosomes modulates allograft rejection1

Pêche, Hélène; Heslan, Michèle; Usal, Claire; Amigorena, Sébastian; Cuturi, María Cristina

doi:10.1097/01.tp.0000092494.75313.38

Cited by 181 publications

(159 citation statements)

References 27 publications

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“…44 G-CSF regulation of CXCR4 has gained much attention as a critical pathway for HSPC release in response to G-CSF. While the role of CXCR4 in the mobilization of myeloid cells, particularly with a contribution of CXCR2, is well-documented, 7,8,10,[13][14][15][16]45 its role in the mobilization of HSPC is not well documented. Previous studies showed that G-CSF administration in man induces a gradual increase in the expression of CXCR4 on bone marrow progenitors (CD34 + or CD38 + cells) over 5 days of treatment.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA126 contributes to granulocyte colony-stimulating factor-induced hematopoietic progenitor cell mobilization by reducing the expression of vascular cell adhesion molecule 1

Salvucci

Jiang²,

Gasperini³

et al. 2012

Haematologica

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The online version of this article has a Supplementary Appendix. BackgroundMobilization of hematopoietic stem/progenitor cells from the bone marrow to the peripheral blood by granulocyte colony-stimulating factor is the primary means to acquire stem cell grafts for hematopoietic cell transplantation. Since hematopoietic stem/progenitor cells represent a minority of all blood cells mobilized by granulocyte colony-stimulating factor, the underlying mechanisms need to be understood in order to develop selective drugs. Design and MethodsWe analyzed phenotypic, biochemical and genetic changes in bone marrow cell populations from granulocyte colony-stimulating factor-mobilized and control mice, and linked such changes to effective mobilization of hematopoietic stem/progenitor cells. ResultsWe show that granulocyte colony-stimulating factor indirectly reduces expression of surface vascular cell adhesion molecule 1 on bone marrow hematopoietic stem/progenitor cells, stromal cells and endothelial cells by promoting the accumulation of microRNA-126 (miR126)-containing microvescicles in the bone marrow extracellular compartment. We found that hematopoietic stem/progenitor cells, stromal cells and endothelial cells readily incorporate these miR126-loaded microvescicles, and that miR126 represses vascular cell adhesion molecule 1 expression on bone marrow hematopoietic stem/progenitor cells, stromal cells and endothelial cells. In line with this, miR126-null mice displayed a reduced mobilization response to granulocyte colony-stimulating factor. ConclusionsOur results implicate miR126 in the regulation of hematopoietic stem/progenitor cell trafficking between the bone marrow and peripheral sites, clarify the role of vascular cell adhesion molecule 1 in granulocyte colony-stimulating factor-mediated mobilization, and have important implications for improved approaches to selective mobilization of hematopoietic stem/progenitor cells.

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Section: Discussionmentioning

confidence: 99%

MicroRNA126 contributes to granulocyte colony-stimulating factor-induced hematopoietic progenitor cell mobilization by reducing the expression of vascular cell adhesion molecule 1

Salvucci

Jiang²,

Gasperini³

et al. 2012

Haematologica

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“…One possibility would be that parenchymal cells acquire sufficient soluble ␤2M, or even intact MHCI contained in exosomes derived from wt hematopoietic cells, to permit direct cytolytic damage. [24][25][26][27] Alternatively, local release of inflammatory mediators, including cytokines and perforin/ granzymes, by CD8 ϩ T cells reacting with host antigen-bearing MHCI ϩ donor APCs may injure bystander MHCI Ϫ tissues. Either effect could be potentiated by underlying damage from irradiation, which disproportionately affects the ears.…”

Section: Discussionmentioning

confidence: 99%

CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL

Matte-Martone

Liu

Jain³

et al. 2008

Blood

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“…Rat bone marrow-derived DCs (BMDCs) were obtained as previously described (15). Briefly, bone marrow cells were cultured in RPMI 1640 complete medium: 10% endotoxin-free FCS (Perbio Science) and 2 mM L -glutamine, 1 mM sodium pyruvate, 1 mM HEPES, and 5 ϫ 10 Ϫ5 M 2-ME (all from Sigma-Aldrich), supplemented with rat IL-4 (4 ng/ml) and murine GM-CSF (1.5 ng/ml).…”

Section: Cell Purification Culture and Activationmentioning

confidence: 99%

The C-Type Lectin-Like Receptor CLEC-1, Expressed by Myeloid Cells and Endothelial Cells, Is Up-Regulated by Immunoregulatory Mediators and Moderates T Cell Activation

Thébault

Lhermite

Tilly

et al. 2009

The Journal of Immunology

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C-type lectin receptors have recently been described as playing crucial roles in immunity and homeostasis since these proteins are able to recognize pathogens as well as self-Ags. We identified the C-type lectin-like receptor-1, CLEC-1, as being overexpressed in a model of rat allograft tolerance. We previously described in this model the expression of numerous cytoprotective molecules by graft endothelial cells and their interplay with regulatory CD4+CD25+ T cells. In this study, we demonstrate that CLEC-1 is expressed by myeloid cells and specifically by endothelial cells in tolerated allografts and that CLEC-1 expression can be induced in endothelial cells by alloantigen-specific regulatory CD4+CD25+ T cells. Analysis of CLEC-1 expression in naive rats demonstrates that CLEC-1 is highly expressed by myeloid cells and at a lower level by endothelial cells, and that its expression is down-regulated by inflammatory stimuli but increased by the immunoregulators IL-10 or TGFβ. Interestingly, we demonstrate in vitro that inhibition of CLEC-1 expression in rat dendritic cells increases the subsequent differentiation of allogeneic Th17 T cells and decreases the regulatory Foxp3+ T cell pool. Additionally, in chronically rejected allograft, the decreased expression of CLEC-1 is associated with a higher production of IL-17. Taken together, our data suggest that CLEC-1, expressed by myeloid cells and endothelial cells, is enhanced by regulatory mediators and moderates Th17 differentiation. Therefore, CLEC-1 may represent a new therapeutic agent to modulate the immune response in transplantation, autoimmunity, or cancer settings.

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Presentation of donor major histocompatibility complex antigens by bone marrow dendritic cell-derived exosomes modulates allograft rejection1

Abstract: The authors demonstrate an effect of allogeneic exosomes on the modulation of immune responses in vivo, suggesting that, like donor cells, exosomes can stimulate or regulate antigen-specific immune responses.

Cited by 181 publications

References 27 publications

MicroRNA126 contributes to granulocyte colony-stimulating factor-induced hematopoietic progenitor cell mobilization by reducing the expression of vascular cell adhesion molecule 1

MicroRNA126 contributes to granulocyte colony-stimulating factor-induced hematopoietic progenitor cell mobilization by reducing the expression of vascular cell adhesion molecule 1

CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL

The C-Type Lectin-Like Receptor CLEC-1, Expressed by Myeloid Cells and Endothelial Cells, Is Up-Regulated by Immunoregulatory Mediators and Moderates T Cell Activation

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