References of "Geenen, Vincent"
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See detailHigh TMEM45A expression is correlated to epidermal keratinization
Hayez, Aurélie; Malaisse, Jérémy; Rogiers, Edith et al

in Experimental Dermatology (in press)

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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 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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See detailEl sindrome tirogastrico autoinmune : sus efectos sobre los micronutrientes y la tumorigenesis gastrica
VALDES SOCIN, Hernan Gonzalo ULg; LUTTERI, Laurence ULg; Cavalier, Etienne ULg et al

in Revista Argentina de Endocrinologia y Metabolismo (2014), 51

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See detailNew Insights into Thymus Physiology
Geenen, Vincent ULg

Scientific conference (2013, November 08)

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See detailProgramming of neuroendocrine self in the thymus and its defect in neuroendocrine autoimmunity
Geenen, Vincent ULg; Bodart, Gwennaëlle ULg; Henry, Séverine et al

in Frontiers in Neuroscience (2013), 7

During centuries after its first description by Galen, the thymus has been considered only as a vestigial endocrine organ until the discovery in 1961 by Jacques FAP Miller of its essential role in the ... [more ▼]

During centuries after its first description by Galen, the thymus has been considered only as a vestigial endocrine organ until the discovery in 1961 by Jacques FAP Miller of its essential role in the development of T (thymo-dependent) lymphocytes. A unique thymus appeared for the first time in cartilaginous fishes some 500 millions years ago, in the same time or shortly after the emergence of the adaptive (acquired) immune system. The thymus may be compared to a small brain or a computer highly specialized in the orchestration of central immunological self-tolerance. This latter was a necessity for the survival of species given the potent evolutionary pressure impacted by the high risk of autotoxicity inherent to the stochastic generation of the diversity of immune cell receptors that characterize the adaptive immune response. The new paradigm of neuroendocrine self-peptides has been proposed together with the definition of neuroendocrine self. Neuroendocrine self-peptides are not secreted by thymic epithelial cells (TECs) according to the classic model of neuroendocrine signaling, but processed for a presentation by, or in association with, the thymic major histocompatibility complex (MHC) proteins. The autoimmune regulator (AIRE) gene/protein controls the transcription of neuroendocrine genes in TECs. The presentation of self-peptides in the thymus is responsible for the clonal deletion of self-reactive T cells emerging during the random recombination of gene segments that encode variable parts of the T cell receptor for the antigen (TCR). In the same time, self-antigen presentation in the thymus also generates regulatory T (Treg) cells that are able to inhibit in the periphery self-reactive T cells having escaped negative selection in the thymus. Several arguments show that the origin of autoimmunity directed against neuroendocrine glands primarily results from a defect in the intrathymic programming of self-tolerance to neuroendocrine functions. This defect may be genetic or acquired during an enteroviral infection, for example. This novel knowledge of normal and pathologic functions of the thymus already constitutes a solid basis for the development of a novel type of tolerogenic/negative self-vaccination against type 1 diabetes (T1D). [less ▲]

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See detailHypothyroïdie infraclinique non auto-immune et statut iodé : étude prospective d'intervention
VALDES SOCIN, Hernan Gonzalo ULg; Tudorescu, A; Lutteri, L et al

in Annales d'Endocrinologie (2013, October), 74

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See detailLe thymus aujourd'hui : d'un organe 'vestigial' à la tolérance au Soi et à l'auto-immunité
Geenen, Vincent ULg

Conference given outside the academic context (2013)

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See detailEvidence for cross-talk between the LH receptor and LH during implantation in mice
Gridelet, Virginie ULg; Tsampalas, Marie; Berndt, Sarah et al

in Reproduction, Fertility and Development (2013), 25

The present study investigated the first interaction that occurs between the blastocyst and endometrium during implantation. Given the ethical objections to studying implantation in humans, a mouse model ... [more ▼]

The present study investigated the first interaction that occurs between the blastocyst and endometrium during implantation. Given the ethical objections to studying implantation in humans, a mouse model was used to study the dialogue between luteinising hormone (LH) and luteinising hormone receptor (LHCGR). Several studies performed on LHCGR-knockout mice have generated controversy regarding the importance of the dialogue between LH and LHCGR during implantation. There has been no demonstration of a bioactive LH-like signal produced by the murine blastocyst. The first aim of the present study was to examine and quantify, using radioimmunoassay, the generation of a bioactive LH signal by the murine blastocyst. We went on to examine and quantify endometrial Lhcgr expression to validate the mouse model. Expression of LHCGR in mouse uteri was demonstrated using immunohistochemistry and western blot analysis. To quantify the expression of Lh in the mouse blastocyst and Lhcgr in the endometrium, reverse transcription–polymerase chain reaction (RT-PCR) and real-time quantitative (q) RT-PCR were performed. The results demonstrate that Lhcgr expression in BALB/c mouse endometrial epithelium is increased at the time of implantation and indicate that LHCGR may contribute to the implantation process. In support of this hypothesis, we identified a bioactive LH signal at the time of murine blastocyst implantation. [less ▲]

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See detailThe actors of human implantation: gametes, embryo and endometrium
Gridelet, Virginie ULg; GASPARD, Olivier ULg; Polese, Barbara ULg et al

in Violin Pereira, Luis Antonio (Ed.) Embryology - Updates and Highlights on Classic Topics (2012)

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See detailPersistent infection of thymic epithelial cells with coxsackievirus B4 results in a decreased expression of insulin-like growth factor 2
Jaïdane, Hela; Caloone, Delphine; Lobert, Pierre-Emmanuel et al

in Journal of Virology (2012), 86

It has been hypothesized that a disturbance of central self-tolerance to islet β-cell may play a role in the enteroviral pathogenesis of type 1 diabetes. Whether enteroviruses can induce an impaired ... [more ▼]

It has been hypothesized that a disturbance of central self-tolerance to islet β-cell may play a role in the enteroviral pathogenesis of type 1 diabetes. Whether enteroviruses can induce an impaired expression of β-cell self-antigens in thymic epithelial cells has been investigated in a murine thymic epithelial (MTE) cell line. This cell line was permissive to the diabetogenic strain CV-B4 E2 and spontaneously expressed type 2 insulin-like growth factor (Igf2), the dominant self-antigen of the insulin family. In this model, a persistent replication of CV-B4 E2 was obtained as attested by the prolonged detection of intracellular positive and negative-strand viral RNA by RT-PCR, and capsid protein VP1 by IF and by the release of infectious particles in culture supernatant fluids. The chronic stage of the infection was characterized by a low proportion of VP1-positive cells (1-2%) whereas many cells harbored enteroviral RNA as displayed by RT-PCR without extraction applied directly on a few cells. Igf2 mRNA and IGF-2 protein were dramatically decreased in CV-B4 E2-infected MTE cultures compared with mock-infected cultures, whereas housekeeping and Il6 genes expression were maintained and Igf1 mRNA was decreased but at a lower extent. Inoculation of CV-B3-, CV-B4 JVB- or Echovirus 1 resulted in a low level of IGF-2 in culture supernatant fluids as well, whereas HSV-1 stimulated the production of the protein. Thus, a persistent infection of a thymic epithelial cell line with enteroviruses, like CV-B4 E2 can result in a disturbed production of IGF-2, a protein involved in central self-tolerance towards islet β-cells. [less ▲]

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See detailManagement of inflammatory bowel disease in pregnancy.
Vermeire, Séverine; Carbonnel, Franck; Coulie, Pierre et al

in Journal of Crohn’s and Colitis [=JCC] (2012), 6(8), 811-23

BACKGROUND AND AIMS: Inflammatory bowel disease (IBD) is a chronic disease affecting mainly young people in their reproductive years. IBD therefore has a major impact on patients' family planning ... [more ▼]

BACKGROUND AND AIMS: Inflammatory bowel disease (IBD) is a chronic disease affecting mainly young people in their reproductive years. IBD therefore has a major impact on patients' family planning decisions. Management of IBD in pregnancy requires a challenging balance between optimal disease control and drug safety considerations. This article aims to provide a framework for clinical decision making in IBD based on review of the literature on pregnancy-related topics. METHODS: Medline searches with search terms 'IBD', 'Crohn's disease' or 'ulcerative colitis' in combination with keywords for the topics fertility, pregnancy, congenital abnormalities and drugs names of drugs used for treatment of IBD. RESULTS: IBD patients have normal fertility, except for women after ileal pouch-anal anastomosis (IPAA) and men under sulfasalazine treatment. Achieving and maintaining disease remission is a key factor for successful pregnancy outcomes in this population, as active disease at conception carries an increased risk of preterm delivery and low birth weight. Clinicians should discuss the need for drug therapy to maintain remission with their patients in order to ensure therapy compliance. Most IBD drugs are compatible with pregnancy, except for methotrexate and thalidomide. If possible, anti-TNF therapy should be stopped by the end of the second trimester and the choice of delivery route should be discussed with the patient. CONCLUSIONS: Disease control prior to conception and throughout pregnancy is the cornerstone of successful pregnancy management in IBD patients. [less ▲]

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See detailExpression of growth hormone (GH)/insulin-like growth factor (IGF) axis during Balb/c ontogeny and effects of GH upon ex-vivo T-cell differentiation
Kermani, Hamid; Goffinet, Lindsay ULg; Mottet, Marie ULg et al

in Neuroimmunomodulation (2012), 19

Aims: We here address the question of expression and role of GH/IGF axis in the thymus. Methods: Using RT-qPCR, the expression profile of various components of the somatotrope GH/IGF axis was measured in ... [more ▼]

Aims: We here address the question of expression and role of GH/IGF axis in the thymus. Methods: Using RT-qPCR, the expression profile of various components of the somatotrope GH/IGF axis was measured in different thymic cell types and during thymus embryogenesis in Balb/c mice. Effect of GH on T-cell differentiation was explored through thymic organotypic culture. Results: Transcription of Gh, Igf1, Igf2 and their related receptors predominantly occurred in thymic epithelial cells (TEC), while a low level of Gh and Igf1r transcription was also evidenced in thymic T cells (thymocytes). Gh, Ghr, Ins2, Igf1, Igf2, and Igfr1, displayed distinct expression profiles depending on the developmental stage. The protein concentration of IGF-1 and IGF-2 were in accordance with the profile of their gene expression. In fetal thymus organ cultures (FTOC) derived from Balb/c mice, treatment with exogenous GH resulted in a significant increase of double negative CD4-CD8- T cells and CD4+ T cells, together with a decrease in double positive CD4+CD8+ T cells. These changes were inhibited by concomitant treatment with GH and GHR antagonist pegvisomant. However, GH treatment also induced a significant decrease in FTOC Gh, Ghr and Igf1 expression. Conclusion: These data show that the thymotropic properties of the somatotrope GH/IGF-1 axis involve an interaction between exogenous GH and GHR expressed by TEC. Since thymic IGF-1 is not increased by GH treatment, the effects of GH upon T-cell differentiation could implicate a different local growth factor or cytokine. [less ▲]

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See detailImmunology in the clinic review series. Focus on type 1 diabetes and virus: enterovirus, thymus and type 1 diabetes pathogenesis
Jaïdane, H.; Sane, F.; Hiar, R. et al

in Clinical & Experimental Immunology (2012), 168

Thymus dysfunction, especially immune suppression, is frequently associated with various virus infections.Whether viruses may disturb the thymus function and play a role in the pathogenesis of autoimmune ... [more ▼]

Thymus dysfunction, especially immune suppression, is frequently associated with various virus infections.Whether viruses may disturb the thymus function and play a role in the pathogenesis of autoimmune diseases is an open issue. Enteroviruses, especially Coxsackievirus B4 (CV-B4), have been largely suggested as potential inducers or aggravating factors of type 1 diabetes (T1D) pathogenesis in genetically predisposed individuals. Several pathogenic mechanisms of enterovirus-induced T1D have been suggested. One of these mechanisms is the impairment of central self-tolerance due to viral infections. Coxsackievirus-B4 is able to infect murine thymus in vitro and in vivo and to infect human thymus in vitro. Thymic epithelial cells and thymocytes are targets of infection with this virus, and several abnormalities, especially disturbance of maturation/differentiation processes, were observed.Altogether, these data suggest that CV-B infection of thymus may be involved in the pathogenesis of T1D. Further investigations are needed to explore this hypothesis. [less ▲]

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