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See detailThe thymus in 2013: from a 'vestigial' organ to immunological self-tolerance and autoimmunity
Geenen, Vincent ULg

in Proceedings of the Belgian Royal Academies of Medicine (2014), 3

The programming of ‘neuroendocrine self’ occurs in the thymus, a cross-talk organ the emergence of which some 450 millions years ago allowed an integrated and harmonious coevolution between the major ... [more ▼]

The programming of ‘neuroendocrine self’ occurs in the thymus, a cross-talk organ the emergence of which some 450 millions years ago allowed an integrated and harmonious coevolution between the major systems of cell-to-cell communication, the nervous, endocrine and immune systems. Neuroendocrine self-peptides are secreted by thymic epithelial cells not according to the classic model of neurosecretion, but are processed for the presentation by, or in association with, the major histocompatibility complex proteins. The autoimmune regulator (Aire) gene/protein controls the transcription of neuroendocrine genes in thymic epithelial cells. The presentation of self-peptides derived from endogenous proteins in the thymus is responsible for the negative selection of self-reactive T cells and, paradoxically in the same time, for the positive selection of thymo- dependant regulatory T (tTreg) cells that can inhibit, in the periphery, those self-reactive T cells that escaped clonal deletion in the thymus. The development of autoimmunity towards endocrine glands first results from a defect in the intrathymic programming of self-tolerance to neuroendocrine functions. This defect may be genetic or acquired, for example during an enteroviral infection. This novel knowledge of normal and pathological functions of the thymus constitutes a solid basis for the development of a novel type of tolerogenic/negative ‘self-vaccination’ against type 1 diabetes. [less ▲]

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See detailHigh TMEM45A expression is correlated to epidermal keratinization
Hayez, Aurélie; Malaisse, Jérémy; Rogiers, Edith et al

in Experimental Dermatology (2014), 23

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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 detailThe appearance of the thymus and the integrated evolution of adaptive immune and neuroendocrine systems
Geenen, Vincent ULg

in Acta Clinica Belgica (2012), 67

The immune system may be considered as a sensory organ able to respond to different kinds of danger signals that are not detected by nervous cells. The immune response is not autonomous but also regulated ... [more ▼]

The immune system may be considered as a sensory organ able to respond to different kinds of danger signals that are not detected by nervous cells. The immune response is not autonomous but also regulated by central and peripheral nervous system, as well as by neuropeptides, vitamin D and neuroendocrine axes such as the corticotrope, somatotrope, thyrotrope and gonadotrope axes. During evolution, the thymus emerged concomitantly with recombinase-dependent adaptive immunity as an ‘immune brain’ or a ‘master class’ highly specialized in the orchestration of central immunological self-tolerance. This was an absolute requirement for survival of species because of the high risk of autotoxicity inherent to the stochastic generation of extreme diversity characterizing this novel adaptive type of immune defenses against non-self. The thymus now appears to be an obligatory intersection for the integrated evolution of the major systems of cell-to-cell signaling, the nervous, endocrine and immune systems. The presentation of many self-peptides by thymic major histocompatibility complex (MHC) proteins is controlled by the autoimmune regulator (AIRE) gene/protein and is responsible for the clonal deletion of self-reactive T cells. In the same time, by still unexplained mechanisms, MHC presentation of the same self-peptides in the thymus promotes the generation of self-specific FOXP3+ CD4+CD25+ natural regulatory T cells (nTreg) that are able to inhibit in periphery self-reactive CD4+ and CD8+ T cells having escaped the thymus censorship. Moreover, a thymus dysfunction is more and more established as the primary event driving the development of organ-specific autoimmunity, which is the tribute paid, mainly by mankind, for the preservation of self against non-self. Our novel knowledge about thymus physiology and physiopathology already serves as the basis for the development of various innovative and efficient immunomodulating strategies in pharmacology. [less ▲]

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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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