References of "Geenen, Vincent"
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See detailTreg, Th17 and γδ T cells during normal and abortive pregnancy
Polese, Barbara ULg; Gridelet, Virginie ULg; Munaut, Carine ULg et al

Poster (2016, January 25)

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See detailSwitch from Hashimoto Thyroiditis (HT) to Graves Basedow (GB) disease : a controlled study in a series of 15 patients
Maiga, I; BETEA, Daniela ULg; Geenen, Vincent ULg et al

in Abstract book - 20th Annual Congress of the Belgian Society of Internal Medicine (2015, December)

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See detailThe central role of the thymus in the programming of immunological tolerance to neuroendocrine self: Implications for the pathogenesis of autoimmune diseases.

Geenen, Vincent ULg

Conference (2015, June)

Our studies have demonstrated that the thymus programs central self-tolerance to neuroendocrine functions through transcription of neuroendocrine-related genes in thymic epithelial cells (TECs). However ... [more ▼]

Our studies have demonstrated that the thymus programs central self-tolerance to neuroendocrine functions through transcription of neuroendocrine-related genes in thymic epithelial cells (TECs). However, thymic neuroendocrine precursors are not secreted but processed as the source of neuroendocrine self-antigens that are presented by thymic proteins of the major histocompatibility complex (MHC). This process, highly specific of the thymus, has allowed an integrated and harmonious coevolution of the neuroendocrine and immune systems when recombination-activating genes and the subsequent adaptive immune response have emerged in cartilaginous fishes some 450-500 millions years ago. All the members of the insulin gene family are expressed in murine TECs under the control of AutoImmune Regulator (AIRE) according a precise hierarchy: Igf2 >Igf1>Ins2>Ins1. Igf2 transcription is defective in TECs of autoimmune diabetes-prone BB rats, and tolerance to insulin is severely impaired in Igf2-/- mice as well as in Igf2-loxP/Foxn1-cre mice with Igf2 deletion targeted in TECs. In addition, the diabetogenic coxsackievirus B4 (CV-B4) is able to persistently infect human and murine TECs and to inhibit Igf2 transcription and IGF-2 synthesis in a murine medullary TEC line (coolaboration with D. Hober, Laboratory of Virology, CHRU and University of Lille 2, France). These studies show that: 1° IGF-2 is the dominant tolerogenic precursor of the family and mediates cross-tolerance to insulin; 2° a thymus dysfunction plays a crucial role in the development of the diabetogenic autoimmune response; and 3° a thymic infection by CV-B4 is implicated in type 1 diabetes (T1D) pathogenesis. Most probably due to its very low level of expression in the thymus, the protein insulin is highly immunogenic and is the primary autoantigen tackled in T1D. On the basis of the tolerogenic properties of IGF-2, we are currently working on the development of a negative/tolerogenic self-vaccine against T1D. [less ▲]

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See detailL'école liégeoise de physiologie aux 19e et 20e siècles
Geenen, Vincent ULg

in Histoire des Sciences Médicales (2015), XLIX(2), 209-218

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See detailAdditional intranasal oxytocin to escitalopram improves depressive symptoms in resistant depression: An open trial.
Scantamburlo, Gabrielle ULg; Hansenne, Michel ULg; Geenen, Vincent ULg et al

in European psychiatry : the journal of the Association of European Psychiatrists (2015), 30(1), 65-68

The aim of this open trial was to assess the antidepressant/anxiolytic effects of oxytocin used as an adjunct to antidepressant in treatment-resistant depression. Fourteen patients, who have not responded ... [more ▼]

The aim of this open trial was to assess the antidepressant/anxiolytic effects of oxytocin used as an adjunct to antidepressant in treatment-resistant depression. Fourteen patients, who have not responded to 40mg of escitalopram, received intranasal synthetic oxytocin during 4 weeks, in association with antidepressant. This is the first open trial study suggesting OT in association with escitalopram significantly reduced scores on Hamilton Depression Rating Scale. [less ▲]

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See detailIntroduction à l'embryologie animale
Geenen, Vincent ULg

Learning material (2015)

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See detailNeuroimmunomodulation in Health and Disease
Geenen, Vincent ULg

Book published by Wiley Company (2015)

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See detailSomatotrope GHRH/GH/IGF-1 axis at the crossroad between immunosenescence and elder frailty
Bodart, Gwennaëlle ULg; Goffinet, Lindsay; Morrhaye, Gabriel et al

in Annals of the New York Academy of Sciences (2015), 1351

Immunosenescence as complex modifications of immunity with age could be related to the so-called frailty syndrome of elderly leading to an inadequate response to minimal aggression. Functional decline ... [more ▼]

Immunosenescence as complex modifications of immunity with age could be related to the so-called frailty syndrome of elderly leading to an inadequate response to minimal aggression. Functional decline, the loss of ability to perform activities of daily living, is related to the decrease in physiological reserves and frailty and is a frequent outcome of hospitalization in older patients. Links between immunosenescence and frailty were explored and 20 immunological parameters were affected in seniors with functional decline. IGF-1, thymopoeisis and telomere length were part of these markers. A strong relationship between insulin-like growth factor-1 (IGF-1) and thymic ouput was evidenced. IGF-1, mediator of GH, was subsequently shown to induce IL-7 secretion in cultured primary human thymic epithelial cells (TECs). We are also exploring the ‘stress hypothesis’ according which an acute stress is the discriminator revealing a frailty susceptility. GH can counteract the deleterious immunosuppressive effect of stress-induced steroids. Under non-stressing conditions, the immunosenescent system preserves physiological responses, while in stressing conditions, the combination of immunosenescence and a defect in somatotrope axis might lead to functional decline. [less ▲]

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See detailHow does thymus infection by coxsackievirus contribute to the pathogenesis of type 1 diabetes?
Michaux, Hélène ULg; Martens, Henri ULg; Jaïdane, Hela et al

in Frontiers in Immunology (2015), 6(Article 338), 1-6

Through synthesis and presentation of neuroendocrine self-antigens by major histocom- patibility complex proteins, thymic epithelial cells (TECs) play a crucial role in programing central immune self ... [more ▼]

Through synthesis and presentation of neuroendocrine self-antigens by major histocom- patibility complex proteins, thymic epithelial cells (TECs) play a crucial role in programing central immune self-tolerance to neuroendocrine functions. Insulin-like growth factor- 2 (IGF-2) is the dominant gene/polypeptide of the insulin family that is expressed in TECs from different animal species and humans. Igf2 transcription is defective in the thymus of diabetes-prone bio-breeding rats, and tolerance to insulin is severely decreased in Igf2−/− mice. For more than 15 years now, our group is investigating the hypothesis that, besides a pancreotropic action, infection by coxsackievirus B4 (CV- B4) could implicate the thymus as well, and interfere with the intrathymic programing of central tolerance to the insulin family and secondarily to insulin-secreting islet β cells. In this perspective, we have demonstrated that a productive infection of the thymus occurs after oral CV-B4 inoculation of mice. Moreover, our most recent data have demonstrated that CV-B4 infection of a murine medullary (m) TEC line induces a significant decrease in Igf2 expression and IGF-2 production. In these conditions, Igf1 expression was much less affected by CV-B4 infection, while Ins2 transcription was not detected in this cell line. Through the inhibition of Igf2 expression in TECs, CV-B4 infection could lead to a breakdown of central immune tolerance to the insulin family and promote an autoimmune response against insulin-secreting islet β cells. Our major research objective now is to understand the molecular mechanisms by which CV-B4 infection of TECs leads to a major decrease in Igf2 expression in these cells. [less ▲]

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See detailEnterovirus persistence as a mechanism in the pathogenesis of type 1 diabetes
Alidjinou, Enagnon Kazali; Sané, Famara; Engelmann, Ilka et al

in Discovery Medicine (2014), 18

Beyond acute clinical conditions, the role of enteroviruses (EVs) in chronic human diseases has been described. Although they are considered as highly cytolytic viruses, EVs can persist in various tissues ... [more ▼]

Beyond acute clinical conditions, the role of enteroviruses (EVs) in chronic human diseases has been described. Although they are considered as highly cytolytic viruses, EVs can persist in various tissues. The persistence is believed to play a major role in the pathogenesis of EV related chronic dis- eases such as type 1 diabetes (T1D). T1D is charac- terized by an autoimmune destruction of pancreatic beta cells, and results from interplay between a genetic predisposition, the immune system, and environmental factors. EVs and especially group B coxsackieviruses (CVB) have been the most incrimi- nated as exogenous agents involved in the develop- ment of T1D. Enteroviral persistence is the result of a virus-host coevolution combining a cell resistance to lysis through mutations or down-regulation of viral receptor, and a decrease of the viral replication by genomic modifications or the production of a sta- ble double-stranded RNA form. CVB can persist in pancreatic cells and therefore could trigger, in genet- ically predisposed individuals, the autoimmune destruction of beta cells mainly through an activa- tion of inflammation. The persistence of the virus in other tissues such as intestine, blood cells, and thy- mus has been described, and could also contribute to some extent to the enteroviral pathogenesis of T1D. The molecular and cellular mechanisms of CVB per- sistence and the link with the development of T1D should be investigated further. [less ▲]

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See detailTreg/Th17 balance during murine embryo implantation and pregnancy
Polese, Barbara ULg; Gridelet, Virginie ULg; Araklioti, Eleni et al

Poster (2014, November)

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See detail9th Congress of the International Society of NeuroImmunoModulation (ISNIM)
Geenen, Vincent ULg

Scientific conference (2014, September 25)

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See detailThe endocrine milieu and CD4 T-lymphocyte polarization during pregnancy
Polese, Barbara ULg; Gridelet, Virginie ULg; Arakioti, Eleni et al

in Frontiers in Endocrinology (2014), 5(Article 106), 1-11

Acceptance of the fetal semi-allograft by the mother’s immune system has become the focus of intensive research. CD4+ T cells are important actors in the establishment of pregnancy. Th1/Th2 paradigm has ... [more ▼]

Acceptance of the fetal semi-allograft by the mother’s immune system has become the focus of intensive research. CD4+ T cells are important actors in the establishment of pregnancy. Th1/Th2 paradigm has been expanded to include CD4+ regulatory T (Treg) and T helper 17 (Th17) cells. Pregnancy hormones exert very significant modulatory properties on the maternal immune system. In this review, we describe mechanisms by which the endocrine milieu modulates CD4 T cell polarization during pregnancy. We first focused on Treg and Th17 cells and on their importance for pregnancy. Secondly, we review the effects of pregnancy hormones [progesterone (P4) and estradiol (E2)] on immune cells previously described, with a particular attention to human chorionic gonadotropin (hCG). The importance of Treg cells for pregnancy is evidenced. They are recruited before implantation and are essential for pregnancy maintenance. Decreased number or less efficient Treg cells are implicated in fertility disorders. As for Th17 cells, the few available studies suggest that they have a negative impact on fertility. Th17 frequency is increased in infertile patients. With the combination of its pro-effects on Th2 and Treg cells and anti-effects on Th1 and Th17 cells, P4 contributes to establishment of a favorable environment for pregnancy. E2 effects are more dependent on the context but it seems that E2 promotes Treg and Th2 cells while it inhibits Th1 cells. hCG positively influences activities of Treg and uterine natural killer cells. This embryo signal is an essential actor for the success of pregnancy, both as the endocrine factor regulating P4 secretion by the ovarian corpus luteum, but also as a paracrine agent during implantation as well as an angiogenic and immunologic mediator during the course of gestation. Luteinizing hormone (LH) immune properties begin to be studied but its positive impact on Treg cells suggests that LH could be a considerable immunomodulator in the mouse. [less ▲]

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See detailProgramming of neuroendocrine self-tolerance in the thymus and its defect in the development of neuroendocrine autoimmunity
Geenen, Vincent ULg

Conference (2014, March 27)

The thymus may be compared to a computer highly specialized in the programming of central immunological self-tolerance. A unique thymus first appeared some 500 million years ago in cartilaginous fishes ... [more ▼]

The thymus may be compared to a computer highly specialized in the programming of central immunological self-tolerance. A unique thymus first appeared some 500 million years ago in cartilaginous fishes, at the same time or shortly after the emergence of the adaptive immune system. A new paradigm of neuroendocrine self-peptides has been proposed, together with the definition of neuroendocrine self. Neuroendocrine self-peptides are secreted by thymic epithelial cells (TECs) not according to the classic model of neurosecretion, but are processed for presentation by the thymic major histocompatibility complex (MHC) machinery. The autoimmune regulator (AIRE) gene/protein controls the transcription of neuroendocrine genes in TECs. Presentation of neuroendocrine self-peptides in the thymus is responsible for the clonal deletion of self-reactive T cells directed toward neuroendocrine antigens, which emerge during the random recombination of gene segments encoding variable parts of the T cell receptor for the antigen (TCR). Quite paradoxically, neuroendocrine self-peptide presentation in the thymus also generates regulatory T (tTreg) cells that inhibit, in the periphery, those self-reactive T cells having escaped thymic negative selection. Several arguments indicate that the origin of autoimmunity directed against neuroendocrine glands results from a primary defect in the intrathymic programming of self-tolerance to neuroendocrine principles. This defect may be genetic or acquired, for example during a viral infection. This novel knowledge of normal and pathologic functions of the thymus constitutes a solid scientific basis for the development of a novel type negative self-vaccination against type 1 diabetes. (Supported by NFSR of Belgium, Wallonia and FP6 Eurothymaide.) [less ▲]

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