Differential down-regulation of HLA-DR on monocyte subpopulations during systemic inflammation

Unit Cytokines & Inflammation, Institut Pasteur, 28 rue Dr, Roux, Paris, France.
Critical care (London, England) 04/2010; 14(2):R61. DOI: 10.1186/cc8959
Source: PubMed

ABSTRACT Decreased expression of human leukocyte antigen class II (HLA-DR) on monocytes is a hallmark of altered immune status in patients with a systemic inflammatory response syndrome (SIRS). So far, the analyses were mainly performed without taking into account monocytes subpopulations.
We studied this modification on CD14HIGH and CD14LOW monocytes of 20 SIRS patients undergoing abdominal aortic surgery (AAS), 20 patients undergoing carotid artery surgery (CAS), and 9 healthy controls, and we investigated mediators and intracellular molecules that may be involved in this process.
HLA-DR on CD14HIGH monocytes started to decrease during surgery, after blood reperfusion, and was further reduced post-surgery. In contrast, HLA-DR expression on CD14LOW cells only decreased after surgery, and to a lesser extent than on CD14HIGH monocytes. Negative correlations were found between the reduction of HLA-DR expression and the change in cortisol levels for both subpopulations, whereas a negative correlation between interleukin-10 (IL-10) levels and HLA-DR modulation was only observed for CD14HIGH cells. In accordance with these ex vivo results, HLA-DR on CD14HIGH and CD14LOW monocytes of healthy donors was reduced following incubation with hydrocortisone, whereas IL-10 only acted on CD14HIGH subpopulation. Furthermore, flow cytometry revealed that the expression of IL-10 receptor was higher on CD14HIGH versus CD14LOW monocytes. In addition, hydrocortisone, and to a lesser extent IL-10, reversed the up-regulation of HLA-DR induced by bacterial products. Finally, membrane-associated RING-CH-1 protein (MARCH1) mRNA, a negative regulator of MHC class II, was up-regulated in monocytes of AAS patients on Day 1 post-surgery, and in those of healthy subjects exposed to hydrocortisone.
This study reveals that HLA-DR expression is modulated differently on CD14HIGH (classical) versus CD14LOW (inflammatory) monocytes after systemic inflammation.

Download full-text


Available from: Minou Adib-Conquy, Jun 28, 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Etching properties of Si substrate by using negative-ion (F<sup>- </sup>) and positive-ion (SF<sub>3</sub><sup>+</sup>) beams were studied. These are dominant ions in pulse-modulated SF<sub>6</sub> plasma with a alternate bias. F<sup>-</sup> ions were extracted from a RF plasma-sputter-type heavy negative ion source by using SF<sub>6</sub> gas as a ionized material. SF<sub>3</sub><sup>+</sup> ion was also extracted from a SF<sub>6</sub> plasma of the source. In the experiment, p-Si substrates and silicon oxides covered with a gold-plated tungsten mesh (100 mesh/inch) were etched by the ion beam at an energy of 50-900 eV with a current density of 3-16 μA/cm<sup>2</sup>. Both etching rates for these ions showed a linear dependence on ion velocity. Chemical sputtering is considered to be dominant process of etching in the low energy range. Threshold etching energies of Si by F<sup>-</sup> was 4.8 eV and larger that 21 eV by SF<sub>3</sub><sup>+</sup>. This is because the molecule ion required dissociation energy. For one fluorine atom at the same velocity in these two ion species, F<sup>-</sup> is considered to have an almost same ability as SF<sub>3</sub><sup>+</sup>
    Ion Implantation Technology Proceedings, 1998 International Conference on; 01/2000
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Studying a large number of patients with sepsis, the Hellenic sepsis study group led by Evangello Giamarellos-Bourboulis emphasizes that the nature of the bacterial infection, its origin (community or nosocomial), its site, and its severity exert different pressures on the immune system. Their study illustrates the heterogeneity of patients with sepsis and points out that numerous key parameters of severe infection influence immune status.
    Critical care (London, England) 06/2010; 14(3):167. DOI:10.1186/cc9046
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Glioblastoma multiforme (GBM) is an aggressive, malignant, and lethal brain tumor, resistant to all current forms of treatment. The rapidly emerging focus on cancer stem cells embodies a paradigm shift in our understanding of tumor pathogenesis, while the development of powerful genome-wide screening techniques has provided cause for optimism related to the development of more reliable therapies primarily targeting GBM stem cells (GBMSCs). There are promising mounting data on providing new molecular targets and predictive markers of response, leading to more effective therapies of GBM, guided by patient-specific genetic and epigenetic profiling. However, the achievement of efficient GBMSC targeting also requires an adequate understanding of the unique microenvironment, and the relationship with the immune system in the central nervous system (CNS) and CNS tumors. The endogenous immune regulation is likely to limit or abrogate the efficacy of the host's immune response, as well as the developed immunotherapeutic strategies at present. Therefore, a comprehensive understanding of the mechanisms underlying the GBM-induced immunosuppression is indispensable. This review presents a summary of the present knowledge both on GBMSCs and the GBM, and/or GBMSC-related mechanisms of developing both local and systemic immunosuppression, of which an understanding may lead to the development of the novel and effective therapeutic strategies.
    The Scientific World Journal 01/2011; 11:930-58. DOI:10.1100/tsw.2011.42 · 1.73 Impact Factor