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See detailIl faut criminaliser les cartels
Neyrinck, Norman ULg

Article for general public (2010)

This article supports the view according to which cartels should be criminalized in EU. Despite their impressive amounts, administrative fines fail to deter collusion. In order to tackle "agency issues ... [more ▼]

This article supports the view according to which cartels should be criminalized in EU. Despite their impressive amounts, administrative fines fail to deter collusion. In order to tackle "agency issues", managers should be held responsible for their involvement in cartels. [less ▲]

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See detailIl faut se méfier du tableau
Guillaume, Jean-François ULg

in Puzzle (2007), 23

Le maintien de toutes les tâches constitutives d’une identité et d’un métier d’élève (s’asseoir sur les bancs de l’école, centrer son attention sur le tableau, écouter le professeur, etc.) se prêt mal aux ... [more ▼]

Le maintien de toutes les tâches constitutives d’une identité et d’un métier d’élève (s’asseoir sur les bancs de l’école, centrer son attention sur le tableau, écouter le professeur, etc.) se prêt mal aux aptitudes requises dans une société de la connaissance. Cette inertie des pratiques scolaires contribuera inévitablement à renforcer l’importance des investissements éducatifs des familles, et les disparités sociales qui les accompagnent. Il paraît en effet bien illusoire de vouloir affronter les nouveaux défis propres aux sociétés de l’information avec le bagage technique et conceptuel d’un mode d’organisation sociale qui s’éteint. [less ▲]

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See detailIl lavoro sul mito nell’epica greca. Letture di Omero e Apollonio. Con una premessa di Diego Lanza
Caneva, Stefano ULg; Tarenzi, Victoria

Book published by ETS (2007)

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See detailIl n'est jamais trop tard pour apprendre à (bien) lire ...
Bruyère, Olivier ULg

in Medi-Sphere (2013), 421

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See detailIl y a 250 ans paraissait "l'Homme machine". La Mettrie (1709-1753). Les origines du materialisme medical
Limet, Raymond ULg

in Revue Médicale de Liège (2000), 55(7), 740-4

Some 250 years ago, the publication of "L'Homme machine" established the fact that human body and brain functioning was to be approached by human study just as like as physics or chemistry.

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See detailIl y a 40 ans, une comète liégeoise
Manfroid, Jean ULg

Article for general public (2012)

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See detailIl y a cent ans, la « Lettre au Roi » de Jules Destrée
Lanneau, Catherine ULg

Article for general public (2012)

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See detailIl y a eu des révolutions avant Twitter et Facebook. Entretien avec François Colmant
Colmant, François ULg

in Wendy Bashi (Ed.) Politique, revue de débats (2012)

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See detailIl y a urgence!
Boularbah, Hakim ULg; Closset-Marchal, Gilberte; de Leval, Georges ULg et al

in Journal des Tribunaux (2009)

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See detailThe IL-10 homologue encoded by cyprinid herpesvirus 3 is essential neither for viral replication in vitro nor for virulence in vivo
Ouyang, Ping ULg; Rakus, Krzysztof ULg; Boutier, Maxime ULg et al

in Veterinary Research (2013)

Cyprinid herpesvirus 3 (CyHV-3), a member of the family Alloherpesviridae, is the causative agent of a lethal disease in common and koi carp. CyHV-3 ORF134 encodes an interleukin-10 (IL-10) homologue. The ... [more ▼]

Cyprinid herpesvirus 3 (CyHV-3), a member of the family Alloherpesviridae, is the causative agent of a lethal disease in common and koi carp. CyHV-3 ORF134 encodes an interleukin-10 (IL-10) homologue. The present study was devoted to this ORF. Transcriptomic analyses revealed that ORF134 is expressed as a spliced gene belonging to the early-late class. Proteomic analyses of CyHV-3 infected cell supernatant demonstrated that the ORF134 expression product is one of the most abundant proteins of the CyHV-3 secretome. To investigate the role of ORF134 in viral replication in vitro and in virulence in vivo, a deleted strain and a derived revertant strain were produced using BAC cloning technologies. The recombinant ORF134 deleted strain replicated in vitro comparably to the parental and the revertant strains. Infection of fish by immersion in water containing the virus induced comparable CyHV-3 disease for the three virus genotypes tested (wild type, deleted and revertant). Quantification of viral DNA by real time TaqMan PCR (in the gills and the kidney) and analysis of carp cytokine expression (in the spleen) by RT-qPCR at different times post-infection did not revealed any significant difference between the groups of fish infected with the three virus genotypes. Similarly, histological examination of the gills and the kidney of infected fish revealed no significant differences between fish infected with ORF134 deleted virus versus fish infected with the control parental or revertant strains. All together, the results of the present study demonstrate that the IL-10 homologue encoded by CyHV-3 is essential neither for viral replication in vitro nor for virulence in common carp. [less ▲]

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See detailIL-4/IL-13 independent goblet cell hyperplasia in experimental helminth infections.
Marillier, Reece G; Michels, Chesney; Smith, Elizabeth M et al

in BMC Immunology (2008), 9

BACKGROUND: Intestinal mucus production by hyperplasic goblet cells is a striking pathological feature of many parasitic helminth infections and is related to intestinal protection and worm expulsion ... [more ▼]

BACKGROUND: Intestinal mucus production by hyperplasic goblet cells is a striking pathological feature of many parasitic helminth infections and is related to intestinal protection and worm expulsion. Induction of goblet cell hyperplasia is associated with TH2 immune responses, which in helminth infections are controlled primarily by IL-13, and also IL-4. In the study presented here we examine the goblet cell hyperplasic response to three experimental parasitic helminth infections; namely Nippostrongylus brasiliensis, Syphacia obvelata and Schistosoma mansoni. RESULTS: As expected N. brasiliensis infection induced a strong goblet cell hyperplasia dependent on IL-4/IL-13/IL-4Ralpha expression. In contrast, and despite previously published transiently elevated IL-4/IL-13 levels, S. obvelata infections did not increase goblet cell hyperplasia in the colon. Furthermore, induction of goblet cell hyperplasia in response to S. mansoni eggs traversing the intestine was equivalent between BALB/c, IL-4/IL-13-/- and IL-4Ralpha-/- mice. CONCLUSION: Together these data demonstrate that intestinal goblet cell hyperplasia can be independent of TH2 immune responses associated with parasitic helminth infections. [less ▲]

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See detailIL-4Ralpha responsive CD4+CD25−CD103+FoxP3− cells control Schistosoma mansoni egg-induced inflammation by secreted IL-10
Dewals, Benjamin G ULg; Hoving, Jennifer C.; Leeto, Mosiuoa et al

Poster (2009, September)

IL-4Ralpha signalling drives Th2-type responses that mediate resistance to parasitic helminth infections. We generated a novel mouse model lacking IL-4Ralpha expression specifically on all T cells ... [more ▼]

IL-4Ralpha signalling drives Th2-type responses that mediate resistance to parasitic helminth infections. We generated a novel mouse model lacking IL-4Ralpha expression specifically on all T cells (iLckcreIl4ra−/lox) to investigate IL-4Ralpha-dependent T cell responses during Schistosoma mansoni egg-driven inflammation. These mice showed higher mortality during acute schistosomiasis compared with Il4ra−/lox controls and previously established CD4+ T cell specific IL-4Ralpha deficient mice (LckcreIl4ra−/lox). iLckcreIl4ra−/lox mice developed a liver restricted pathology associated with drastic reductions of both Th2/type 2 responses and alternative macrophage activation within the granulomas. Additionally, iLckcreIl4ra−/lox mice had (i) increased FoxP3+ Treg cell responses in the granulomas, which was explained by IL-4 mediated inhibition of FoxP3 induction, and (ii) reduction of antigen-specific production of IL-10 by CD4+CD103+FoxP3− cells. In a footpad model of S. mansoni egg-induced inflammation with subsequent IL-10 neutralisation and adoptive cell transfer experiments we found evidence that the increased inflammation in iLckcreIl4ra−/lox mice was due to the impaired development of IL-10-secreting CD4+CD25−CD103+FoxP3− cells. Together, these data demonstrate that IL-4Ralpha responsiveness by T cells promote IL-10-secreting CD4+CD25−CD103+FoxP3− cells and alternatively activated macrophages, which act in concert to control egg-induced inflammation. [less ▲]

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See detailIL-4Ralpha responsiveness by T cells prevents peripheral induction of FoxP3-expressing regulatory T cells during TH2-polarized immune response
Dewals, Benjamin G ULg; Brombacher, Frank

Conference (2008, March 12)

Survival from Schistosoma mansoni infection requires the development of a finely regulated TH2-polarized immune response driven by the parasite egg antigens. A number of studies have proposed that S ... [more ▼]

Survival from Schistosoma mansoni infection requires the development of a finely regulated TH2-polarized immune response driven by the parasite egg antigens. A number of studies have proposed that S. mansoni egg antigens induce peripheral FoxP3-expressing regulatory T cells involved in the modulation of pro-inflammatory T helper immune responses (1-3). However, the tight regulation between antagonistic TH1, TH2 and Treg developmental programs in response to S. mansoni egg-antigens remains poorly understood. In this study, we demonstrated in vitro that IL-4 strongly inhibits TGF1-induced FoxP3 expression by naive T cells and this inhibition is dependent on IL-4R expression on T cells. Surprisingly, wild-type mice that developed a strong TH2 immune response to S. mansoni egg antigens were able to modulate the magnitude of egg-induced inflammation in contrast to mice disrupted of IL-4R globally or specifically on T cells. The TH2 response developed by wild-type mice also prevented the induction of FoxP3-expressing CD4+ T cells in the draining lymph node. This was not apparent in LckcreIL-4R-/lox or IL-4R-/- mice. In addition, IL-4 neutralization in vivo promoted the induction of FoxP3+CD4+ cells in the draining lymph node. Finally, IL-4 responsiveness by T cells induced a CD103-expressing CD4+ T cell population which produced IL-10 in response to egg antigens. Consequently, our study shows that the modulation of egg-induced inflammation is independent of FoxP3-expressing regulatory T cells but highlights a potential role of CD103-expressing CD4+ T cells as IL-10 producing regulatory T cells. [less ▲]

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See detailIL-4Ralpha responsiveness of non-CD4 T cells contributes to resistance in schistosoma mansoni infection in pan-T cell-specific IL-4Ralpha-deficient mice.
Dewals, Benjamin G ULg; Hoving, Jennifer C; Leeto, Mosiuoa et al

in American Journal of Pathology (2009), 175(2), 706-16

Interleukin (IL)-4 and IL-13 are T helper 2 cytokines whose biological functions are induced through a common IL-4 receptor alpha chain (IL-4Ralpha). CD4(+) T cell-specific IL-4Ralpha-mediated signaling ... [more ▼]

Interleukin (IL)-4 and IL-13 are T helper 2 cytokines whose biological functions are induced through a common IL-4 receptor alpha chain (IL-4Ralpha). CD4(+) T cell-specific IL-4Ralpha-mediated signaling drives susceptibility to Leishmania major infection, but is not essential to host survival following Schistosoma mansoni infection. Here we generated a novel mouse model lacking IL-4Ralpha expression specifically on all T cells (iLck(cre)Il4ra(-/lox)), which was compared with CD4(+) T cell-specific IL-4Ralpha-deficient mice (Lck(cre)Il4ra(-/lox)), to investigate the possible roles of IL-4Ralpha responsive non-CD4(+) T cells during either L. major or S. mansoni infection. Our results demonstrate a successful generation of transgene-bearing hemizygous iLck(cre)Il4ra(-/lox) BALB/c mice that have effective deletion of IL-4Ralpha on all T-cell populations. We show that iLck(cre)Il4ra(-/lox) mice infected with L. major developed a healing disease phenotype as previously observed in Lck(cre)Il4ra(-/lox) mice, demonstrating that absence of IL-4Ralpha-responsive non-CD4(+) in addition to CD4(+) T cells does not further affect transformation of BALB/c to a healer phenotype. In acute schistosomiasis, however, iLck(cre)Il4ra(-/lox) mice showed enhanced mortality compared with Il4ra(-/lox) and Lck(cre)Il4ra(-/lox) mice. iLck(cre)Il4ra(-/lox) mice died with similar kinetics to highly susceptible Il4ra(-/-) mice, despite controlling gut inflammation. In addition, iLck(cre)Il4ra(-/lox) mice presented increased liver granuloma sizes, as compared with Lck(cre)Il4ra(-/lox) mice, with similar eosinophils, fibrosis, and liver damage. In conclusion, IL-4Ralpha-responsive non-CD4(+) T cells prolong survival to acute schistosomiasis and contribute to the better control of hepatic granulomatous inflammation. [less ▲]

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See detailIL-4Ralpha-associated antigen processing by B cells promotes immunity in Nippostrongylus brasiliensis infection.
Horsnell, William G. C.; Darby, Matthew G.; Hoving, Jennifer C. et al

in PLoS pathogens (2013), 9(10), 1003662

In this study, B cell function in protective T(H)2 immunity against N. brasiliensis infection was investigated. Protection against secondary infection depended on IL-4Ralpha and IL-13; but not IL-4 ... [more ▼]

In this study, B cell function in protective T(H)2 immunity against N. brasiliensis infection was investigated. Protection against secondary infection depended on IL-4Ralpha and IL-13; but not IL-4. Protection did not associate with parasite specific antibody responses. Re-infection of B cell-specific IL-4Ralpha(-)/(-) mice resulted in increased worm burdens compared to control mice, despite their equivalent capacity to control primary infection. Impaired protection correlated with reduced lymphocyte IL-13 production and B cell MHC class II and CD86 surface expression. Adoptive transfer of in vivo N. brasiliensis primed IL-4Ralpha expressing B cells into naive BALB/c mice, but not IL-4Ralpha or IL-13 deficient B cells, conferred protection against primary N. brasiliensis infection. This protection required MHC class II compatibility on B cells suggesting cognate interactions by B cells with CD4(+) T cells were important to co-ordinate immunity. Furthermore, the rapid nature of these protective effects by B cells suggested non-BCR mediated mechanisms, such as via Toll Like Receptors, was involved, and this was supported by transfer experiments using antigen pulsed Myd88(-)/(-) B cells. These data suggest TLR dependent antigen processing by IL-4Ralpha-responsive B cells producing IL-13 contribute significantly to CD4(+) T cell-mediated protective immunity against N. brasiliensis infection. [less ▲]

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See detailIL-4Ralpha-independent expression of mannose receptor and Ym1 by macrophages depends on their IL-10 responsiveness.
Dewals, Benjamin G ULg; Marillier, Reece G; Hoving, Jennifer C et al

in PLoS Neglected Tropical Diseases (2010), 4(5), 689

IL-4Ralpha-dependent responses are essential for granuloma formation and host survival during acute schistosomiasis. Previously, we demonstrated that mice deficient for macrophage-specific IL-4Ralpha ... [more ▼]

IL-4Ralpha-dependent responses are essential for granuloma formation and host survival during acute schistosomiasis. Previously, we demonstrated that mice deficient for macrophage-specific IL-4Ralpha (LysM(cre)Il4ra(-/lox)) developed increased hepatotoxicity and gut inflammation; whereas inflammation was restricted to the liver of mice lacking T cell-specific IL-4Ralpha expression (iLck(cre)Il4ra(-/lox)). In the study presented here we further investigated their role in liver granulomatous inflammation. Frequencies and numbers of macrophage, lymphocyte or granulocyte populations, as well as Th1/Th2 cytokine responses were similar in Schistosoma mansoni-infected LysM(cre)Il4ra(-/lox) liver granulomas, when compared to Il4ra(-/lox) control mice. In contrast, a shift to Th1 responses with high IFN-gamma and low IL-4, IL-10 and IL-13 was observed in the severely disrupted granulomas of iLck(cre)Il4ra(-/lox) and Il4ra(-/-) mice. As expected, alternative macrophage activation was reduced in both LysM(cre)Il4ra(-/lox) and iLck(cre)Il4ra(-/lox) granulomas with low arginase 1 and heightened nitric oxide synthase RNA expression in granuloma macrophages of both mouse strains. Interestingly, a discrete subpopulation of SSC(high)CD11b+I-A/I-E(high)CD204+ macrophages retained expression of mannose receptor (MMR) and Ym1 in LysM(cre)Il4ra(-/lox) but not in iLck(cre)Il4ra(-/lox) granulomas. While aaMphi were in close proximity to the parasite eggs in Il4ra(-/lox) control mice, MMR+Ym1+ macrophages in LysM(cre)Il4ra(-/lox) mice were restricted to the periphery of the granuloma, indicating that they might have different functions. In vivo IL-10 neutralisation resulted in the disappearance of MMR+Ym1+ macrophages in LysM(cre)Il4ra(-/lox) mice. Together, these results show that IL-4Ralpha-responsive T cells are essential to drive alternative macrophage activation and to control granulomatous inflammation in the liver. The data further suggest that in the absence of macrophage-specific IL-4Ralpha signalling, IL-10 is able to drive mannose receptor- and Ym1-positive macrophages, associated with control of hepatic granulomatous inflammation. [less ▲]

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