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See detailNovel perspectives in the pathogenesis of type 1 diabetes
Geenen, Vincent ULg

Conference (2005, November)

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See detailOxytocin receptor pattern of expression in primary lung cancer and in normal human lung
Pequeux, Christel ULg; Breton, C.; Hagelstein, M. T. et al

in Lung Cancer (2005), 50(2), 177-188

In order to assess if oxytocin- and vasopressin-induced mitogenic effects detected on small-cell lung carcinoma (SCLC) cell lines could be transposed on primary SCLC, the aim of the present work was to ... [more ▼]

In order to assess if oxytocin- and vasopressin-induced mitogenic effects detected on small-cell lung carcinoma (SCLC) cell lines could be transposed on primary SCLC, the aim of the present work was to identify mediators of these mitogenic actions on primary tumours samples. This was addressed on normal human lung tissue, on SCLC and on non-SCLC (NSCLC). Herein, we observe, in normal human lung, that OTR is colocalized with vascular endothelial cells of the lung and is not expressed by lung cells of epithelial nature. We detected mRNA amplification of V1aR, V2R and of a V2R variant. We observed that 86% of SCLC biopsies analyzed expressed at least the OTR and that 71% expressed the OTR, the V1aR and the V2R altogether. Comparatively, 50% of NSCLC biopsies tested expressed at least the OTR and 32% expressed the OTR, the V1aR and the V2R altogether. The occurrence of the V1bR/V3R is of 28 and 18% for SCLC and NSCLC, respectively. Nevertheless, for the SCLC biopsies analyzed in this study, V1bR/V3R expression correlates, in all cases, with the expression of all the other neurohypophysial peptide receptors. Our results suggest that neurohypophysial peptide antagonists may offer promise as a potential new therapeutic modality for the treatment of lung cancer expressing at least one of the neurhypophysial peptide receptor subtypes. (c) 2005 Elsevier Ireland Ltd. All rights reserved. [less ▲]

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See detailOntogenesis and functional aspects of oxytocin and vasopressin gene expression in the thymus network
Hansenne, Isabelle ULg; Rasier, G.; Pequeux, Christel ULg et al

in Journal of Neuroimmunology (2005), 158(1-2), 67-75

Ontogenesis of oxytocin (OT) and vasopressin (VP) gene expression and function were investigated in murine thymus. OT and VP transcripts were detected in the thymus on embryonic days 13 and 15 ... [more ▼]

Ontogenesis of oxytocin (OT) and vasopressin (VP) gene expression and function were investigated in murine thymus. OT and VP transcripts were detected in the thymus on embryonic days 13 and 15, respectively. Corresponding messenger RNAs were evidenced in thymic epithelial cells by in situ hybridization with a neurophysin probe. From all OT and VP receptors, only OTR was expressed by all T-cell subsets, while V1bR was found in double positive and single positive CD8 cells. In fetal thymic organ cultures, OTR antagonist d[DTyr(Et)(2), Thr(4)]OVT increased early apoptosis of CD8 cells, while V1bR antagonist (Sanofi SSR 149415) inhibited T-cell differentiation, and favored CD8 T-cell commitment. (C) 2004 Elsevier B.V. All rights reserved. [less ▲]

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See detailNouvelles donnees sur la pathogenie du diabete de type 1
Geenen, Vincent ULg; Brilot, F.; Louis, Céline ULg et al

in Revue Médicale de Liège (2005), 60(5-6, May-Jun), 291-6

The autoimmune nature of the diabetogenic process and the major contribution of T lymphocytes stand now beyond any doubt. However, despite the identification of the three major type 1-diabetes-related ... [more ▼]

The autoimmune nature of the diabetogenic process and the major contribution of T lymphocytes stand now beyond any doubt. However, despite the identification of the three major type 1-diabetes-related autoantigens (insulin, GAD65 and phosphatase IA-2), the origin of this immune dysregulation still remains unknown. More and more evidence supports a thymic dysfunction in the establishment of central self-tolerance to the insulin family as a crucial factor in the development of the autoimmune response selective of pancreatic insulin-secreting islet beta cells. All the genes of the insulin family (INS, IGF1 and IGF2) are expressed in the thymus network. However, IGF-2 is the dominant member of this family first encountered by T cells in the thymus, and only IGFs control early T-cell differentiation. IGF2 transcription is defective in the thymus in one animal model of type 1 diabetes, the Bio-Breeding (BB) rat. The sequence B9-23, one dominant autoantigen of insulin, and the homologous sequence B11-25 derived from IGF-2 exibit the same affinity and fully compete for binding to DQ8, one class-II major histocompatibility complex (MHC-II) conferring major genetic susceptibility to type 1 diabetes. Compared to insulin B9-23, the presentation of IGF-2 B11-25 to peripheral mononuclear cells (PBMCs) isolated from type 1 diabetic DQ8+ adolescents elicits a regulatory/tolerogenic cytokine profile (*IL-10, *IL-10/IFN-g, *IL-4). Thus, administration of IGF-2 derived self-antigen(s) might constitute a novel form of vaccine/immunotherapy combining both an antagonism for the site of presentation of a susceptible MHC allele, as well as a downstream tolerogenic/regulatory immune response. [less ▲]

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See detailLe role des virus dans la pathogenie du diabete de type 1
Brilot, F.; Geenen, Vincent ULg

in Revue Médicale de Liège (2005), 60(5-6, May-Jun), 297-302

The precise role of viral infections in the pathogenesis of type 1 diabetes is still the subject of an important discussion. Coxsackievirus B4 (CVB4) is the virus the most implicated by a series of ... [more ▼]

The precise role of viral infections in the pathogenesis of type 1 diabetes is still the subject of an important discussion. Coxsackievirus B4 (CVB4) is the virus the most implicated by a series of epidemiological studies. Pathogenic mechanisms underlying such a relationship implicate a molecular mimicry between CVB4 sequences and beta-cell autoantigens, but mainly a persistent CVB4 infection of pancreatic beta cells followed by a release of sequestered beta antigens and a "bystander" activation of autoreactive T cells. The demonstration of intrathymic expression of antigens specific of peripheral tissues has opened a novel research perspective. We have shown that CVB4 is able to infect in a persistent and producive manner human thymic epithelial cell cultures and human fetal thymic lobes in organotypic cultures. This infection induces an important thymic dysfunction characterized by a severe depletion of thymocytes (thymic T cells) and an up-regulated expression by thymic epithelial and T cells of class I proteins encoded by the major histocompatibility complex (MHC-I). Such thymic dysfunction might be responsible for a decrease of beta-cell central self-tolerance and anti-CVB4 cytotoxic CD8 T-cell activity. CVB4-induced thymic dysfunction would contribute in close association with the peripheral "bystander" effect to the destruction of insulin-secreting islet beta cells and to the development of type 1 diabetes. [less ▲]

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See detailCoxsackievirus B4 and type 1 diabetes
Brilot, Fabienne; Geenen, Vincent ULg; Hober, Didier

in Thebault, Sabine (Ed.) Progress in Virus Research (2005)

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See detailThymus self-antigens as a way for restoring self-tolerance in type 1 diabetes
Geenen, Vincent ULg

in Journal of NeuroImmunoModulation (2005)

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See detailAn insulin-like growth factor 2-derived self-antigen inducing a regulatory cytokine profile after presentation to peripheral blood mononuclear cells from DQ8(+) type 1 diabetic adolescents - Preliminary design of a thymus-based tolerogenic self-vaccination
Geenen, Vincent ULg; Louis, Céline ULg; Martens, Henri ULg

in Annals of the New York Academy of Sciences (2004), 1037

This work aims to evaluate the potential use of insulin-like growth factor 2 (IGF-2) as the dominant thymic self-antigen precursor of the insulin family in designing a tolerogenic approach to type 1 ... [more ▼]

This work aims to evaluate the potential use of insulin-like growth factor 2 (IGF-2) as the dominant thymic self-antigen precursor of the insulin family in designing a tolerogenic approach to type 1 diabetes (T1D) prevention. This evaluation was primarily based on cytokine profile driven by MHC presentation of insulin and IGF-2-derived antigens to PBMC cultures derived from 16 T1D DQ8(+) adolescents. Insulin B9-23, one dominant P-cell autoantigen, and the homologous sequence B11-25 of IGF-2 display the same affinity and fully compete for binding to DQ8, a MHC-II allele conferring major genetic susceptibility to type 1 diabetes (T1D). However, compared to insulin beta 9-23, presentation of IGF-2 B11-25 elicits a suppressive/regulatory cytokine profile with a higher number of IL-10-secreting cells (P < 0.05), a much higher ratio of IL-10/IFN-gamma (P < 0.01), as well as a lower number of IL-4-secreting cells (P < 0.05). Thus, with regard to T1D prevention, administration of IGF-2-derived self-antigen(s) seems to be an efficient approach that combines both antagonism for binding to a major susceptibility MHC-II allele, as well as downstream promotion of an antigen-driven tolerogenic response. [less ▲]

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See detailOxytocin- and vasopressin-induced growth of human small-cell lung cancer is mediated by the mitogen-activated protein kinase pathway
Pequeux, Christel ULg; Keegan, B. P.; Hagelstein, M. T. et al

in Endocrine-Related Cancer (2004), 11(4), 871-885

Malignant growth of small-cell lung carcinoma is promoted by various neuroendocrine autocrine/paracrine loops. Therefore, to interfere with this mitogenic process, it is crucial to elucidate the ... [more ▼]

Malignant growth of small-cell lung carcinoma is promoted by various neuroendocrine autocrine/paracrine loops. Therefore, to interfere with this mitogenic process, it is crucial to elucidate the mechanisms involved. It is known that the oxytocin (OT) and vasopressin (VP) genes, normally transcriptionally restricted in their expression, are activated in small-cell lung cancer (SCLC), concomitantly with expression of their receptors (OTR, V1aR, V1bR/V3R and V2R). The aim of the present study was to characterize, in concentrations close to physiological and pharmacological conditions, intracellular signalling events triggered by OT and VP binding to their specific receptors in SCLC cells and to identify factors mediating OT- and VP-induced mitogenic effects on SCLC. Known agonists for OTR ([Thr(4),GlY(7)]OT) and V1aR (F180), in addition to OT and VP, were able to elicit increases in cytosolic Ca2+ levels and this effect could be blocked using an OTR antagonist (OVTA) or a V1aR antagonist (SR49059) respectively. There was no activation of the cAMP pathway detected after VP, dDAVP (a V2R agonist), or OT treatment. Stimulation of SCLC cells with OT and VP led to an increase of extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, maximal at 5 min, and the subsequent phosphorylation of its downstream target p90 ribosomal S6 kinase (p90(RSK)). Pre-incubation with OVTA and SR49059, and with inhibitors of phospholipase C (PLC), protein kinase C (PKC), mitogen-activated protein kinase/ERK kinase (MEK) 1/2 and a Ca2+ chelator significantly reduced OT- and VP-induced ERK1/2 phosphorylations. OVTA, SR49059 as well as MEK1/2 and PKC inhibitors also downregulated OT- and VP-induced p90RSK phosphorylation. In [H-3]thymidine-uptake 2, experiments, we subsequently observed that PLC, Ca2+, PKC and ERK1/2 are absolutely required for the OT- and VP-stimulated SCLC cellular growth process. In conclusion, the results presented here indicate that OT- and VP-induced mitogenic effects on SCLC are respectively mediated by OTR and V1aR signalling and that this mitogenic signalling passes through the phosphorylation of ERK1/2 and p90(RSK) in a PLC-, Ca2+-, PKC- and MEK1/2-dependent pathway. [less ▲]

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See detailHuman chorionic gonadotropin and growth factors at the embryonic-endometrial interface control leukemia inhibitory factor (LIF) and interleukin 6 (IL-6) secretion by human endometrial epithelium
PERRIER d'HAUTERIVE, Sophie ULg; Charlet, Jeanne de Chantal ULg; Berndt, Sarah ULg et al

in Human Reproduction (2004), 19(11), 2633-2643

BACKGROUND: The elucidation of the molecular mechanisms by which the embryo contributes to its implantation is an area of extensive research. The main objective of this study was to investigate the ... [more ▼]

BACKGROUND: The elucidation of the molecular mechanisms by which the embryo contributes to its implantation is an area of extensive research. The main objective of this study was to investigate the pattern of leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) secretion by human endometrial epithelium, and their regulation by human chorionic gonadotropin (hCG) and other growth factors present at the embryonic-endometrial interface. METHODS: Endometrial epithelial cells (EEC) were isolated from biopsies collected at both proliferative and secretory phases of fertile women. RESULTS: HCG (1-50 IU/ml) increased LIF secretion by EEC cultures derived from follicular phase (up to 285+/-75%) or from secretory phase (up to 212+/-16%). In contrast, hCG reduced IL-6 secretion by EEC in both phases. The hCG/LH receptor gene was transcribed by EEC as evidenced by RT-PCR. Insulin-like growth factors 1 and 2 increased LIF secretion by EEC. Transforming growth factor beta1 stimulated LIF and reduced IL-6 secretion. CONCLUSIONS: Through hCG, the blastocyst may be involved in the control of its implantation (via an increase of proimplantatory LIF) and tolerance (via an inhibition of proinflammatory IL-6). Other growth factors present at the embryonic-endometrial interface are also involved in the control of LIF and IL-6 endometrial secretion. [less ▲]

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See detailThe presentation of self in the thymus network: a novel way for prevention and cure of autoimmune diseases
Geenen, Vincent ULg

in Journal of Neuroimmunology (2004, September), 154

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See detailEuro-Thymaide website and EDTSA, the European Database of Thymus Self-Antigens
Geenen, Vincent ULg

Textual, factual or bibliographical database (2004)

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See detailNeurohypophysial Receptor Gene Expression by Thymic T Cell Subsets and Thymic T Cell Lymphoma Cell Lines
Hansenne, Isabelle ULg; Rasier, G.; Charlet-Renard, C. et al

in Clinical & Developmental Immunology (2004), 11(1), 45-51

Neurohypophysial oxytocin (OT) and vasopressin (VP) genes are transcribed in thymic epithelium, while immature T lymphocytes express functional neurohypophysial receptors. Neurohypophysial receptors ... [more ▼]

Neurohypophysial oxytocin (OT) and vasopressin (VP) genes are transcribed in thymic epithelium, while immature T lymphocytes express functional neurohypophysial receptors. Neurohypophysial receptors belong to the G protein-linked seven-transmembrane receptor superfamily and are encoded by four distinct genes, OTR, V1R, V2R and V3R. The objective of this study was to identify the nature of neurohypophysial receptor in thymic T cell subsets purified by immunomagnetic selection, as well as in murine thymic lymphoma cell lines RL12-NP and BW5147. OTR is transcribed in all thymic T cell subsets and T cell lines, while V3R transcription is restricted to CD4+CD8+ and CD8+ thymic cells. Neither V1R nor V2R transcripts are detected in any kind of T cells. The OTR protein was identified by immunocytochemistry on thymocytes freshly isolated from C57BL/6 mice. In murine fetal thymic organ cultures, a specific OTR antagonist does not modify the percentage of T cell subsets, but increases late T cell apoptosis further evidencing the involvement of OT/OTR signaling in the control of T cell proliferation and survival. According to these data, OTR and V3R are differentially expressed during T cell ontogeny. Moreover, the restriction of OTR transcription to T cell lines derived from thymic lymphomas may be important in the context of T cell leukemia pathogenesis and treatment. [less ▲]

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See detailImmunoendocrinology in Health and Disease
Geenen, Vincent ULg; Chrousos, George

Book published by Marcel Dekker (2004)

L'objectif de cet ouvrage est d'illustrer l'importance de l'immunoendocrinologie pour la compréhension de la pathogénie et le traitement des endocrinopathies auto-immunes, et des maladies inflammatoires ... [more ▼]

L'objectif de cet ouvrage est d'illustrer l'importance de l'immunoendocrinologie pour la compréhension de la pathogénie et le traitement des endocrinopathies auto-immunes, et des maladies inflammatoires, infectieuses, allergiques et néoplasiques, de même que le processus d'immunosénescence. Des experts internationaux de chaque domaine ont rédigé des chapitres à propos de maladies chroniques qui ont un impact majeur tant émotionnel qu'économique sur la société humaine. [less ▲]

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See detailPresentation of neuroendocrine self in the thymus: toward a novel type of vaccine/immunotherapy
Geenen, Vincent ULg; Brilot, Fabienne; Hansenne, Isabelle et al

in Drug Design Reviews - Online (2004), 1

Slightly after the emergence some 400 millions years ago of the first signs of adaptive immune response, tolerogenic pathways developed in order to preserve the integrity of self from potential autoimmune ... [more ▼]

Slightly after the emergence some 400 millions years ago of the first signs of adaptive immune response, tolerogenic pathways developed in order to preserve the integrity of self from potential autoimmune toxicity. Amongst those tolerogenic pathways, the thymus occupies a central place both by deleting self-reactive T cells that are produced in the thymus during random recombination of gene segments encoding the variable parts of the T-cell receptor for antigen (TCR) (negative selection), and by generating self-antigen specific regulatory T cells (Tr). A repertoire of neuroendocrine-related genes are transcribed by thymic stromal cells — epithelial and ‘nurse’ cells (TEC/TNC), dendritic cells (DC) and macrophages (MF) — in such a way that a dominant protein precursor is expressed in the thymus environment. Oxytocin (OT) and neurokinin A (NKA) are the dominant thymic precursors for the neurohypophysial hormone and tachykinin families, respectively. With regard to the insulin gene family, all members are transcribed following a precise cell topography and hierarchy in the profile of gene expression: IGF2 (TEC/TNC) > IGF1 (MF) >> INS (medullary TEC and/or DC). This hierarchy implies that IGF-2 is more tolerated than IGF-1, and much more than Insulin (Ins). The low level of INS transcription in the thymus also explains why Ins displays immunogenic properties, as well as the significant prevalence (±40%) of anti-Ins autoantibodies in the general population. Ins administration failed in providing tolerance or protection toward islet ß cells in type 1 diabetes (T1D). In contrast, the presentation of IGF-2 B11-25, the homologous sequence of Ins B9-23, to peripheral blood mononuclear cells (PBMC) isolated from DQ8+ T1D adolescents significantly increases IL-10 secretion and IL10 expression. Given the potent regulatory/suppressive properties of IL-10 on the autoimmune response toward islet ß cells, these data support that IGF-2 derived sequences constitute a strong basis for the development of an antigen-specific driven tolerogenic approach for T1D prevention and/or cure. [less ▲]

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See detailNouvelles approches du diagnostic et de la pathogénie du diabète de type 1
Geenen, Vincent ULg

in Louvain Medical (2004), 123

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See detailCoxsackievirus B4 infection of human fetal thymus cells
Brilot, Fabienne; Geenen, Vincent ULg; Hober, Didier et al

in Journal of Virology (2004), 78(18), 9854-9861

The infection of human fetal thymus organ cultures (FTOC) with coxsackievirus B4 E2 (CVB4 E2) was investigated. Both positive- and negative-strand viral RNA were detected by real-time quantitative reverse ... [more ▼]

The infection of human fetal thymus organ cultures (FTOC) with coxsackievirus B4 E2 (CVB4 E2) was investigated. Both positive- and negative-strand viral RNA were detected by real-time quantitative reverse transcription-PCR (RT-PCR) in CVB4 E2-infected FTOC, which supported high yields of virus production (similar to10(6) 50% tissue culture infective doses/ml), and in flow-sorted thymocyte populations for 7 days after inoculation. Cortical CD4(+) CD8(+) thymocytes were found to be the principal targets of infection. Inoculation of human FTOC with CVB4 E2 led to a marked and progressive depletion of immature thymocytes (CD4(+) CD8(+) cells) with no enhancement of Annexin V-positive cells. CVB4 E2 replication caused significant major histocompatibility complex (MHC) class I upregulation on these cells. MHC class I upregulation was correlated with positive- and negative-strand RNA quantitative detection and the release of infectious particles. In addition, chloroquine treatment of FTOC and single-thymocyte suspensions suggested that MHC class I upregulation on thymocytes was the result of direct infection rather than caused by production of soluble factors such as alpha interferon. Thus, CVB4 E2 can infect human fetal thymocytes, which subsequently results in quantitative and qualitative abnormalities of these cells. [less ▲]

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See detailThe central role of the thymus in the development of self-tolerance and autoimmunity in the neuroendocrine system
Geenen, Vincent ULg; Brilot, Fabienne; Hansenne, Isabelle et al

in Geenen, Vincent; Chrousos, Geroge P. (Eds.) Immunoendocrinology in Health and Disease (2004)

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See detailThymus and T cells
Geenen, Vincent ULg; Brilot, Fabienne; Hansenne, Isabelle et al

in Smith, Barry H.; Adelman, George (Eds.) Encyclopedia of Neuroscience, 3rd Edition (2004)

Evidence for intimate interconnections between the three major systems of cell communication, the nervous, endocrine and immune systems, has opened important novel research perspectives. Neuroimmune ... [more ▼]

Evidence for intimate interconnections between the three major systems of cell communication, the nervous, endocrine and immune systems, has opened important novel research perspectives. Neuroimmune-endocrine interactions are now established as crucial factors for the control of body development and homeostasis. In distant species and invertebrates, the foundations of both the neuroendocrine system and innate immunity were coexisting until now without any apparent problem. Some 400 millions years ago, in a relatively short period after agnathan fishes (e.g., hagfish and lamprey), adaptive immunity emerged in the first gnathostomes, cartilaginous fishes (e.g., shark and ray). Somatic recombination machinery characterizes adaptive immunity and is responsible for the random generation of the huge diversity of immune receptors able to recognize infectious antigens. The emergence of this novel form of immune defenses exerted a so potent pressure that structures and mechanisms developed along the paths of lymphocyte traffic to impose immunological self-tolerance, that is, the inability of the immune system to attack the host organism. Together with the generation of diversity and memory, self-tolerance constitutes a fundamental property of the immune system. The progressive rise in the level of immune diversity and complexity also explains why self-tolerance failures (i.e., organ-specific autoimmune diseases) were increasingly detected during evolution, the maximum being currently observed in the human species. The first thymus appeared in cartilaginous fishes (chondrichthyes), concomitantly with the emergence of rudimental forms of adaptive immunity. Though some forms of tolerance induction already takes place in primary hemopoietic sites (fetal liver and bone marrow), antigen-dependent B-cell tolerance is primarily due to an absence of T-cell help. Among all lymphoid structures, the thymus is the only organ specialized in the establishment of central self-tolerance. The thymus crucially stands at the crossroad between the immune and neuroendocrine systems. In this organ responsible for thymopoiesis—T-cell generation—(Kong et al., 1998), the neuroendocrine system regulates the process of T-cell differentiation from the very early stages. In addition, T lymphocytes undergo inside the thymus a complex educative process that establishes central T-cell self-tolerance of neuroendocrine principles (Geenen et al., 1992; Martens et al., 1996). Within the thymus, a confrontation permanently occurs between previously established neuroendocrine principles and a recent system equipped with recombination machinery promoting stochastic generation of response diversity. Contrary to a previous assumption, the thymus functions throughout life (Poulin et al., 1999; Geenen et al., 2003) and plays a fundamental role in the recovery of a competent T-cell repertoire after intensive chemotherapy or during highly active antiretroviral therapy (Mackall et al., 1995; Douek et al., 1998). [less ▲]

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See detailL'implantation: premier dialogue entre la mère et l'embryon
Geenen, Vincent ULg

Conference (2003, September)

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