H Ansart-Pirenne

Hôpital Universitaire Robert Debré, Lutetia Parisorum, Île-de-France, France

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Publications (10)30.14 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The authors studied the relationship between the dynamics of Epstein-Barr virus (EBV) load, CD8 T-cell activation and differentiation, and EBV-associated symptoms in 25 children after kidney transplantation (Tx). Twenty-two patients were enrolled at the time of Tx and three at diagnosis of EBV-induced post-transplant lymphoproliferative disease (PTLD). EBV load was serially measured by a semiquantitative method of DNA amplification in blood cells. The percentages of activated (human leukocyte antigen-DR) and of effector-memory (CD28) CD8 circulating cytolytic T lymphocytes (CTL) were serially evaluated by flow cytometry. The cytotoxic potential of CTL was assessed by a CD3-redirected cytotoxic assay. For three children with post-Tx uncomplicated primary EBV infection, EBV load peaked by months 1 to 2 after Tx and declined spontaneously by months 3 to 6, whereas expansion of activated and effector-memory CTL was absent (one case) or transient and moderate (two cases). In 15 patients who were EBV-seropositive before Tx and who did not develop EBV-PTLD, transient elevation of EBV load but no noticeable changes in CTL phenotype were observed. In contrast, in one child who was also EBV-seropositive before Tx but who developed EBV-PTLD, a major and sustained elevation of EBV load and of activated and effector-memory CTL was observed. In three patients retrospectively enrolled at diagnosis of EBV-PTLD, sustained elevation of both viral load and activated T cells was also noticed. Finally, increased cytotoxic activity correlated with increased level of activated CTL. An association between high and sustained T-cell activation, EBV load, and the occurrence of EBV-PTLD was observed. Furthermore, intense cytotoxic activity was observed in EBV-PTLD, with favorable outcome.
    Transplantation 07/2004; 77(11):1706-13. · 3.78 Impact Factor
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    ABSTRACT: Improvements in HLA-typing by DNA-based methods now allow accurate genotyping of unrelated bone marrow (UBM) donors and recipients and also definition of haplotypes. In this regard, B*5002 has been predicted in linkage disequilibrium with Cw*0602, DRB1*0406 and DQB1*0402 based on the frequency of allele coexistence. Here, we confirm this assumption by HLA genotyping of four informative families and three unrelated individuals. In the four families, the extended haplotype HLA-B*5002, -Cw*0602, -DRB1*0406, DQB1*0402 can be definitely assigned by the mode of heritance. Furthermore, this association of alleles was also found in the three B*5002 unrelated individuals. Knowledge of the frequent linkage disequilibrium of these rare alleles can improve UBM donor search strategies.
    Tissue Antigens 03/2001; 57(2):163-6. · 2.93 Impact Factor
  • Transplantation Proceedings 01/2001; 32(8):2757-9. · 0.95 Impact Factor
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    ABSTRACT: We report the association of neurological and intestinal disorders with the reactivation of Epstein-Barr virus (EBV) in a child. This previously healthy 13-yr-old boy presented with pharyngitis and acute abdominal ileus. Laparotomy excluded a mechanical obstruction. Postoperatively, he suffered from prolonged intestinal obstruction, pandysautonomia, and encephalomyelitis. Histological examination of the appendix and a rectal biopsy taken 3 months after the onset showed an absence of ganglion cells (appendix) and hypoganglionosis (rectum), with a mononucleate inflammatory infiltrate in close contact with the myenteric neural plexuses. EBV-PCR was positive in the blood and cerebrospinal fluid, and in situ hybridization with the Epstein-Barr virus encoded RNA probe showed positive cells throughout the appendix wall including the myenteric area, in a mesenteric lymph node, and in the gastric biopsies. EBV spontaneous lymphocytic proliferation was noted in the blood. The serology for EBV showed previous infection but anti-early antigen antibodies were present. No immunodeficiency was found. Neurological and GI recovery occurred after 6 months of parenteral nutrition and bethanechol. The omnipresence of EBV associated with the neurointestinal symptoms suggest that the virus was the causal agent. This is the first documented case of acquired hypoganglionnosis due to EBV reactivation.
    The American Journal of Gastroenterology 02/2000; 95(1):280-4. · 9.21 Impact Factor
  • N Soulimani, H Ansart-Pirenne, O Sibony, P Blot, G Sterkers
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    ABSTRACT: Here we show that Fas ligand, a death factor that plays a key role in peripheral T cell tolerance and homeostasis, can be induced in peripheral blood mononuclear cells from both newborns (cord) and adults. Indeed, stimulation of both populations by ionomycin and phorbol 12-myristate 13-acetate or through the T cell receptor (anti-CD3) leads to a selective lysis of targets transfected with Fas but not of the parental cell line. This lysis clearly involves a Fas-based mechanism inasmuch as it was correlated with the appearance of Fas ligand transcripts and competitively inhibited by a Fas-Fc fusion protein. Yet, the use of separated T cell populations revealed that both CD4+ and CD8+ T cells express this function in adults whereas the CD4 subset is primarily involved in lysis by a Fas-based mechanism in cord. Altogether these results suggest that distinct T cell subsets might be recruited to exert Fas-based lysis during T cell ontogeny. Furthermore, it is tempting to speculate that CD4+ T cells are primarily involved in peripheral T cell homeostasis and tolerance in early life because they are committed to exert Fas-based lysis before any antigen-priming. Finally, the model of Fas ligand exploration described herein might be of great help for the identification of Fas ligand dysregulation in various diseases in infants, including those patients with autoimmune lymphoproliferative syndrome in which Fas is functional.
    Pediatric Research 09/1999; 46(2):239-44. · 2.67 Impact Factor
  • H Ansart-Pirenne, N Soulimani, E Tartour, P Blot, G Sterkers
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    ABSTRACT: Here we confirmed that IL2 mRNA expression in CD3-stimulated T cells is defective at birth. Because protein-tyrosine phosphorylation is an important part of signaling through CD3 and plays a key role in IL2 transcription, we further investigated whether impaired IL2 response to CD3 in newborns would be accompanied with an alteration of tyrosine phosphorylation. In this purpose, CD3-induced tyrosine phosphorylation was evaluated comparatively in newborn and adult cells by immunoblotting of total cellular extract with an antiphosphotyrosine antibody. Results show that, in both peripheral lymphocytes or purified CD4 T cells from both cord and adult, CD3 stimulation could induce small even significant tyrosine-phosphorylation. Tyrosine phosphorylation occurs as soon as 2' following CD3 ligation and was still evident up to 15-20'. Yet, by using a highly sensitive method to analyze CD3-induced accumulation of phosphorylated substrates, which consisted in adding pervanadate, an inhibitor of phosphatases, during the last 2 min of CD3 stimulation, we showed that the intensity of tyrosine phosphorylation was clearly decreased in cord cells. From these results, it is tempting to speculate that suboptimal capacities of cord T cells to up-regulate tyrosine phosphorylation might contribute to defective IL2 production in neonates.
    Pediatric Research 04/1999; 45(3):409-13. · 2.67 Impact Factor
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    ABSTRACT: The precise mechanism by which pretransplant blood transfusions may favorably influence the graft outcome in human transplantation remains unknown. Here, we explored whether the mechanism might be related to an alteration of cytokine response to transplantation antigens. Eight patients awaiting kidney transplantation were selected to receive a single planned pretransplant blood transfusion. Before transfusion and 7 days after transfusion, peripheral blood mononuclear cells from these patients were isolated and in vitro stimulated in a one-way mixed leukocyte reaction (MLR) by using allogeneic fixed Epstein Barr virus-transformed cells as stimulators. The use of a semiquantitative reverse-transcriptase polymerase chain reaction cycle technique to analyze cytokine mRNAs revealed that allostimulation by donor cells clearly induced accumulation of interleukin (IL)-2, IL-4, interferon (IFN)-gamma, and IL-10 mRNA in peripheral blood mononuclear cells collected both before and after transfusion (eight of eight patients). However, both T helper 1 (IFN-gamma) and T helper 2 (IL-4) cytokine responses were more elevated after transfusion in eight of eight patients, as were IL-2 responses in five of eight patients. Such up-regulation of cytokine responses by transfusion was mostly directed against blood donor cells. Indeed, after stimulation by third-party cells, this up-regulation was both inconstant (two of three patients) and of less intensity, and no change was detected after stimulation by autologous cells (three of three patients). That IL-2, IL-4, and IFN-gamma responses to donor cells were increased by transfusion was further supported by results on cytokine secretion showing increased levels of IL-2 (P < 0.05), IFN-gamma (P = 0.054), and IL-4 (P < 0.05) proteins in supernatants of posttransfusion MLR as compared with pretransfusion MLR. In contrast, transfusion-induced changes in the amount of IL-10 mRNAs were not obvious and were quite variable from one patient to another.
    Transplantation 09/1998; 66(3):376-84. · 3.78 Impact Factor
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    ABSTRACT: Background. The precise mechanism by which pre-transplant blood transfusions may favorably influence the graft outcome in human transplantation remains unknown. Here, we explored whether the mechanism might be related to an alteration of cytokine response to transplantation antigens. Methods. Eight patients awaiting kidney transplantation were selected to receive a single planned pretransplant blood transfusion. Before transfusion and 7 days after transfusion, peripheral blood mononuclear cells from these patients were isolated and in vitro stimulated in a one-way mixed leukocyte reaction(MLR) by using allogeneic fixed Epstein Barr virus-transformed cells as stimulations. Results. The use of a semiquantitative reverse-transcriptase polymerase chain reaction cycle technique to analyze cytokine mRNAs revealed that allostimulation by donor cells clearly induced accumulation of interleukin(IL)-2, IL-4, interferon (IFN)-γ, and IL-10 mRNA in peripheral blood mononuclear cells collected both before and after transfusion (eight of eight patients). However, both T helper 1 (IFN-γ) and T helper 2 (IL-4) cytokine responses were more elevated after transfusion in eight of eight patients, as were IL-2 responses in five of eight patients. Such up-regulation of cytokine responses by transfusion was mostly directed against blood donor cells. Indeed, after stimulation by third-party cells, this up-regulation was both inconstant (two of three patients) and of less intensity, and no change was detected after stimulation by autologous cells (three of three patients). Conclusions. That IL-2, IL-4, and IFN-γ responses to donor cells were increased by transfusion was further supported by results on cytokine secretion showing increased levels of IL-2 (P<0.05), IFN-γ(P=0.05), and IL-4 (P<0.05) proteins in supernatants of posttransfusion MLR as compared with pretransfusion MLR. In contrast, transfusion-induced changes in the amount of IL-10 mRNAs were not obvious and were quite variable from one patient to another.
    Transplantation 08/1998; 66(3):376-384. · 3.78 Impact Factor
  • Archives de Pédiatrie 02/1998; 5(2):218-218. · 0.36 Impact Factor
  • R. Novo, V. Baudouin, H. Ansart-Pirenne, C. Loirat, G. Sterkers
    Archives De Pediatrie - ARCHIVES PEDIATRIE. 01/1998; 5(7):821-821.