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Open AccessResearch article

Direct contact of platelets and their released products exert different effects on human dendritic cell maturation

Hind Hamzeh-Cognasse1 email, Fabrice Cognasse1,2 email, Sabine Palle3 email, Patricia Chavarin2 email, Thomas Olivier3 email, Olivier Delézay1 email, Bruno Pozzetto1 email and Olivier Garraud1,2 email

Mucosal Immunity and Pathogen Agents Group (GIMAP-EA3064), Faculty of Medicine, Jean Monnet University of Saint-Etienne, Saint-Etienne, France

Auvergne-Loire Regional Blood Bank (EFS Auvergne-Loire), Saint-Etienne, France

4D Multiphotonic Confocal Microscopy Platform, (Hubert Curien Laboratory and UMR CNRS 5516), Jean Monnet University of Saint-Etienne, Saint-Etienne, France

author email corresponding author email

BMC Immunology 2008, 9:54doi:10.1186/1471-2172-9-54

Published: 25 September 2008

Abstract

Background

Dendritic cells (DCs) are antigen presenting cells capable of inducing innate and adaptive immune responses. According to the stimulus and their maturation state, DCs induce immunogenic or tolerogenic responses. Platelets (PLTs), which are involved in haemostasis and inflammation, can also interact with DCs. In this study, we examined the effect of PLTs on DC maturation in vitro. Human monocyte-derived DCs were co-cultured for 2 days with homologous PLTs either in the same well or in 0.4 μm-pore size filter-separated compartments.

Results

Confocal microscopy showed the attachment of PLTs to DC membranes. The DC receptor involved in this interactions was found to be CD162. In addition, we observed that DCs co-cultured with PLTs in filter-separated compartments acquired a mature phenotype (high CD80, CD86, and intermediate CD83 expression; IL-12(p70) production; efficient stimulation of autologous CD4+ T cell proliferation), while DCs co-cultured with PLTs in the same compartment did not undergo phenotypic maturation, did not secrete IL-12(p70) or IL-1β, but instead induced moderate Th2-polarized T cell proliferation.

Conclusion

These data indicate that (i) PLTs secrete a soluble DC-activating factor that was demonstrated not to be soluble CD40-Ligand (CD154; as could have been expected from in vivo and previous in vitro work) but to be nucleotide, and (ii) that cell-to-cell contact did not induce DC maturation, possibly because nucleotide release by PLTs was prevented by direct contact with DCs. This work demonstrates that PLTs are active elements of the immune system that might play a role in balancing the ability of DCs to polarize T cell responses, therefore making them critical factors in transfusion processes.


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