References of "Desmet, Christophe"
     in
Bookmark and Share    
Peer Reviewed
See detailRelease and innate immune detection of host cell DNA mediate the adjuvant activity of aluminum salts
Marichal, Thomas ULg; Ohata, K; Bedoret, D et al

Poster (2011)

Detailed reference viewed: 12 (1 ULg)
Peer Reviewed
See detailRelease and innate immune detection of host cell DNA mediate the adjuvant activity of aluminum salts
Marichal, Thomas ULg; Ohata, K; Bedoret, Denis et al

Conference (2011)

Detailed reference viewed: 6 (1 ULg)
Peer Reviewed
See detailSelf-DNA release mediates the adjuvant effects of aluminum salts
Marichal, Thomas ULg; Ohata, K; Bedoret, Denis et al

Poster (2011)

Detailed reference viewed: 2 (0 ULg)
Full Text
See detailInvestigation of the innate immunity in the lower respiratory tract in exercising horses
Frellstedt, Linda ULg; Gosset, Philippe; Desmet, Christophe ULg et al

in Proceedings of the 1st Scientific Meeting of the Faculty of Veterinary Medicine (2011)

Detailed reference viewed: 35 (8 ULg)
Peer Reviewed
See detailInterferon Response Factor 3 is required for airway allergy to house dust mite in mice
Marichal, Thomas ULg; Bedoret Denis; Mesnil, Claire ULg et al

in Short Book of the Annual Congress of the Euopean Respiratory Society (ERS), Barcelone (2010, September)

Detailed reference viewed: 18 (4 ULg)
Peer Reviewed
See detailRelease and innate detection of hot cell DNA mediates the adjuvant effects of aluminium salts on adaptive responses.
Marichal, Thomas ULg; Ohata, Keichii; Bedoret, Denis et al

Conference (2010, February)

Detailed reference viewed: 12 (0 ULg)
Full Text
See detailLes macrophages interstitiels, gardiens de l'homeostasie immune pulmonaire.
Bedoret, Denis; Bureau, Fabrice ULg; Desmet, Christophe ULg

in Medecine Sciences : M/S (2010), 26(3), 229-31

Detailed reference viewed: 56 (19 ULg)
Full Text
Peer Reviewed
See detailViral induction of Zac1b through TLR3- and IRF3-dependent pathways
Warzée, Barbara ULg; Mesnil, Claire ULg; Hober, D. et al

in Molecular Immunology (2010), 48(1-3), 119-127

Zinc finger protein regulator of apoptosis and cell cycle arrest (Zac1) is a transcription factor able to induce apoptosis or cell cycle arrest through independent pathways. In spite of the important ... [more ▼]

Zinc finger protein regulator of apoptosis and cell cycle arrest (Zac1) is a transcription factor able to induce apoptosis or cell cycle arrest through independent pathways. In spite of the important potential functions attributed to Zac1, little is known of its physiological regulation and biological function. We discovered that variant Zac1b was expressed in murine embryonic fibroblasts (MEFs) treated with polyriboinosinic polyribocytidylic acid [poly(I:C)], a synthetic double-stranded RNA. This regulation occurred mainly through Toll-Like Receptor 3 (TLR3)- and Interferon Regulatory Factor 3 (IRF3)-dependent pathways. As TLR3 and IRF3 are central activators of antiviral immunity, we hypothesized that Zac1 may be implicated in antiviral responses. In line with this notion, we observed that Zac1b was expressed in MEFs infected with Encephalomyocarditis virus (EMCV). We also observed that Zac1-deficient MEFs were less sensitive to EMCV-induced cell death than wild-type MEFs. However, Zac1 gene inactivation had no effect on the survival of mice infected with EMCV. In conclusion, this study describes for the first time a transcriptional regulation of Zac1b, induced by synthetic dsRNA and RNA viruses, the functional significance of which remains to be further investigated. [less ▲]

Detailed reference viewed: 61 (20 ULg)
Full Text
Peer Reviewed
See detailInterferon Response Factor 3 is essential for house dust mite-induced airway allergy
Marichal, Thomas ULg; Bedoret, Denis; Mesnil, Claire ULg et al

in Journal of Allergy and Clinical Immunology (The) (2010), 126(4), 836-844

IRF3, mainly known as a central orchestrator of antiviral responses, is required for proallergic functions of dendritic cells in response to aeroallergens. Thus, this study demonstratively identifies a ... [more ▼]

IRF3, mainly known as a central orchestrator of antiviral responses, is required for proallergic functions of dendritic cells in response to aeroallergens. Thus, this study demonstratively identifies a new pathway potentially implicated in the etiology of airway allergy [less ▲]

Detailed reference viewed: 103 (38 ULg)
Peer Reviewed
See detailIRF3 is required for induction of allergic airway inflammation by dendritic cells
Marichal, Thomas ULg; Bedoret, Denis; Goriely, S et al

Poster (2009)

Detailed reference viewed: 10 (0 ULg)
Full Text
Peer Reviewed
See detailIRF3 is required for the induction of allergic airway inflammation by lung dendritic cells in a mouse model of house dust mite-induced atopic asthma
Marichal, Thomas ULg; Bedoret, Denis; Goriely, M. et al

in Abstracts of the 17th Annual European Respiratory Society Congress, Vienna, Austria (2009)

Detailed reference viewed: 43 (14 ULg)
Peer Reviewed
See detailIRF3 is required for induction of allergic airway inflammation by dendritic cells
Marichal, Thomas ULg; Bedoret, Denis; Goriely, M. et al

Conference (2009)

Detailed reference viewed: 45 (11 ULg)
Full Text
Peer Reviewed
See detailLung interstitial macrophages alter dendritic cell functions to prevent airway allergy in mice
Bedoret, Denis ULg; Wallemacq, Hugues ULg; Marichal, Thomas ULg et al

in Journal of Clinical Investigation (2009), 119(12), 3723-38

The respiratory tract is continuously exposed to both innocuous airborne antigens and immunostimulatory molecules of microbial origin, such as LPS. At low concentrations, airborne LPS can induce a lung DC ... [more ▼]

The respiratory tract is continuously exposed to both innocuous airborne antigens and immunostimulatory molecules of microbial origin, such as LPS. At low concentrations, airborne LPS can induce a lung DC-driven Th2 cell response to harmless inhaled antigens, thereby promoting allergic asthma. However, only a small fraction of people exposed to environmental LPS develop allergic asthma. What prevents most people from mounting a lung DC-driven Th2 response upon exposure to LPS is not understood. Here we have shown that lung interstitial macrophages (IMs), a cell population with no previously described in vivo function, prevent induction of a Th2 response in mice challenged with LPS and an experimental harmless airborne antigen. IMs, but not alveolar macrophages, were found to produce high levels of IL-10 and to inhibit LPS-induced maturation and migration of DCs loaded with the experimental harmless airborne antigen in an IL-10-dependent manner. We further demonstrated that specific in vivo elimination of IMs led to overt asthmatic reactions to innocuous airborne antigens inhaled with low doses of LPS. This study has revealed a crucial role for IMs in maintaining immune homeostasis in the respiratory tract and provides an explanation for the paradox that although airborne LPS has the ability to promote the induction of Th2 responses by lung DCs, it does not provoke airway allergy under normal conditions. [less ▲]

Detailed reference viewed: 187 (68 ULg)
Peer Reviewed
See detailFra-1 and its associated transcriptome are central determinants of human breast cancer metastasis
Desmet, Christophe ULg; Prieur, A; Reyal, F et al

Poster (2008)

Detailed reference viewed: 11 (1 ULg)
Full Text
Peer Reviewed
See detailOncogene-induced senescence relayed by an interleukin-dependent inflammatory network.
Kuilman, Thomas; Michaloglou, Chrysiis; Vredeveld, Liesbeth C. W. et al

in Cell (2008), 133(6), 1019-1031

Oncogene-induced cellular senescence (OIS) is emerging as a potent cancer-protective response to oncogenic events, serving to eliminate early neoplastic cells from the proliferative pool. Using combined ... [more ▼]

Oncogene-induced cellular senescence (OIS) is emerging as a potent cancer-protective response to oncogenic events, serving to eliminate early neoplastic cells from the proliferative pool. Using combined genetic and bioinformatic analysis, we find that OIS is linked specifically to the activation of an inflammatory transcriptome. Induced genes included the pleiotropic cytokine interleukin-6 (IL-6), which upon secretion by senescent cells acted mitogenically in a paracrine fashion. Unexpectedly, IL-6 was also required for the execution of OIS, but in a cell-autonomous mode. Its depletion caused the inflammatory network to collapse and abolished senescence entry and maintenance. Furthermore, we demonstrate that the transcription factor C/EBPbeta cooperates with IL-6 to amplify the activation of the inflammatory network, including IL-8. In human colon adenomas, IL-8 specifically colocalized with arrested, p16(INK4A)-positive epithelium. We propose a model in which the context-dependent cytostatic and promitogenic functions of specific interleukins contribute to connect senescence with an inflammatory phenotype and cancer. [less ▲]

Detailed reference viewed: 9 (1 ULg)
Full Text
Peer Reviewed
See detailDendritic cells genetically engineered to express IL-10 induce long-lasting antigen-specific tolerance in experimental asthma.
Henry, E.; Desmet, Christophe ULg; Garze, V. et al

in Journal of Immunology (2008), 181(10), 7230-7242

Dendritic cells (DCs) are professional APCs that have a unique capacity to initiate primary immune responses, including tolerogenic responses. We have genetically engineered bone marrow-derived DCs to ... [more ▼]

Dendritic cells (DCs) are professional APCs that have a unique capacity to initiate primary immune responses, including tolerogenic responses. We have genetically engineered bone marrow-derived DCs to express the immunosuppressive cytokine IL-10 and tested the ability of these cells to control experimental asthma. A single intratracheal injection of OVA-pulsed IL-10-transduced DCs (OVA-IL-10-DCs) to naive mice before OVA sensitization and challenge prevented all of the cardinal features of airway allergy, namely, eosinophilic airway inflammation, airway hyperreactivity, and production of mucus, Ag-specific Igs, and IL-4. OVA-IL-10-DCs also reversed established experimental asthma and had long-lasting and Ag-specific effects. We furthermore showed, by using IL-10-deficient mice, that host IL-10 is required for mediating the immunomodulatory effects of OVA-IL-10-DCs and demonstrated a significant increase in the percentage of OVA-specific CD4(+)CD25(+)Foxp3(+)IL-10(+) regulatory T cells in the mediastinal lymph nodes of OVA-IL-10-DC-injected mice. Finally, adoptive transfer of CD4(+) mediastinal lymph node T cells from mice injected with OVA-IL-10-DCs protected OVA-sensitized recipients from airway eosinophilia upon OVA provocation. Our study describes a promising strategy to induce long-lasting Ag-specific tolerance in airway allergy. [less ▲]

Detailed reference viewed: 57 (15 ULg)
Full Text
Peer Reviewed
See detailStat5 Is an Ambivalent Regulator of Neutrophil Homeostasis
Fievez, Laurence ULg; Desmet, Christophe ULg; Henry, Emmanuelle et al

in PLoS ONE (2007), 2(1), 727

Although STAT5 promotes survival of hematopoietic progenitors, STAT5-/- mice develop mild neutrophilia. METHODOLOGY/PRINCIPAL FINDINGS: Here, we show that in STAT5-/- mice, liver endothelial cells (LECs ... [more ▼]

Although STAT5 promotes survival of hematopoietic progenitors, STAT5-/- mice develop mild neutrophilia. METHODOLOGY/PRINCIPAL FINDINGS: Here, we show that in STAT5-/- mice, liver endothelial cells (LECs) autonomously secrete high amounts of G-CSF, allowing myeloid progenitors to overcompensate for their intrinsic survival defect. However, when injected with pro-inflammatory cytokines, mutant mice cannot further increase neutrophil production, display a severe deficiency in peripheral neutrophil survival, and are therefore unable to maintain neutrophil homeostasis. In wild-type mice, inflammatory stimulation induces rapid STAT5 degradation in LECs, G-CSF production by LECs and other cell types, and then sustained mobilization and expansion of long-lived neutrophils. CONCLUSION: We conclude that STAT5 is an ambivalent factor. In cells of the granulocytic lineage, it exerts an antiapoptotic function that is required for maintenance of neutrophil homeostasis, especially during the inflammatory response. In LECs, STAT5 negatively regulates granulopoiesis by directly or indirectly repressing G-CSF expression. Removal of this STAT5-imposed brake contributes to induction of emergency granulopoiesis. [less ▲]

Detailed reference viewed: 89 (39 ULg)
Full Text
Peer Reviewed
See detailDe novo C16- and C24-ceramide generation contributes to spontaneous neutrophil apoptosis.
Seumois, Gregory; Fillet, Marianne ULg; Gillet, Laurent ULg et al

in Journal of Leukocyte Biology (2007), 81(6), 1477-1486

Neutrophils rapidly undergo spontaneous apoptosis following their release from the bone marrow. Although central to leukocyte homeostasis, the mechanisms that regulate neutrophil apoptosis remain poorly ... [more ▼]

Neutrophils rapidly undergo spontaneous apoptosis following their release from the bone marrow. Although central to leukocyte homeostasis, the mechanisms that regulate neutrophil apoptosis remain poorly understood. We show here that apoptosis of cultured neutrophils is preceded by a substantial increase in the intracellular levels of 16 and 24 carbon atom (C(16)- and C(24))-ceramides, which are lipid second messengers of apoptosis and stress signaling. Treatment of neutrophils with fumonisin B(2), a selective inhibitor of the de novo pathway of ceramide synthesis, prevented accumulation of C(16)- and C(24)-ceramides. Moreover, fumonisin B(2) significantly reduced caspase-3, -8, and -9 activation and apoptosis in these cells. Conversely, 3-O-methylsphingomyelin and fantofarone, which are specific inhibitors of neutral and acid sphingomyelinases, respectively, neither inhibited C(16)- and C(24)-ceramide production nor decreased the apoptosis rate in neutrophils, indicating that in these cells, ceramides are not generated from membrane sphingomyelin. Further experiments showed that increasing endogenous C(16)- and C(24)-ceramide levels by using DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol and (1S,2R)-D-erythro-2-(N-myristoylamino)-1-phenyl-1-propanol, two inhibitors of ceramide metabolism, enhances caspase-3, -8, and -9 activity and increases neutrophil apoptosis. Similarly, apoptosis was induced rapidly when synthetic C(16)- and/or C(24)-ceramides were added to neutrophil cultures. Finally, GM-CSF, a cytokine that delays neutrophil apoptosis, abrogated C(16)- and C(24)-ceramide accumulation totally in cultured neutrophils, whereas Fas ligation accelerated apoptosis in these cells without affecting de novo ceramide production. We conclude that de novo generation of C(16)- and C(24)-ceramides contributes to spontaneous neutrophil apoptosis via caspase activation and that GM-CSF exerts its antiapoptotic effects on neutrophils, at least partly through inhibition of ceramide accumulation. [less ▲]

Detailed reference viewed: 48 (12 ULg)