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  • Phone : +33 2 40 08 74 16
  • Location : Nantes, France
Last update 2014-06-19 18:42:20.727

Beatrice CHARREAU • PhD in Immunology

Course and current status

  • Senior Scientist in Vascular Immunobiology and  Transplant Immunology at INSERM UMR-S 1064, Centre de Recherche INSERM en Transplantation et Immunologie (CRTI), Nantes, France.
  • Principal investigator/ Co-Head of INSERM UMR1064  team 5 “Endothelial and Glomerular dysfunction: mechanisms and therapeutic targets ”
  • Partner in two Laboratories of Excellence (LabEx) fundings: LabEx IGO ImmunoGraft Oncology and LabEx Transplantex.
  • Partner in the European  Center for Transplantation Sciences and Immunotherapy (CESTI)


- 2007 : Qualification to the degree of University Professor in Cell Biology.

- 2001 : Qualification to the degree of University Assistant Professor in Cell Biology.

- 2000: “Ability to direct Research” (H D R), University of Nantes, France.

- 1996: PhD in Immunology , University of Nantes, France

- 1991: Engineering degree in Biochemistry, Conservatoire National des Arts et Métiers,  Paris, France

- 1987: Bachelor degree in Science and Technics in Biochemistry, Conservatoire National des Arts    et Métiers , Tours

- 1980: Higher Technician Certificate (BTS) in Biochemistry. Ecole Nationale de Chimie, Paris.


  • Member of The Transplantation Society (TTS)
  • Member of the American Society for Biochemistry and Molecular Biology (ASBMB)
  • Member of the Société de Néphrologie
  • Member of the Société de Biologie Cellulaire de France (SBCF)
  • Member of Biomedical Research International Editorial board

Scientific summary

Effectors and mechanisms of endothelial dysfunction in Transplantation-  Béatrice Charreau

The roles that the tightly regulated expression of class I-like MHC molecules on graft’s endothelial cells (EC) may play in both innate and acquired allogeneic response remain to be elucidated (reviewed in Coupel S. et al. Cur. Op. Org. Transplant. 2006). Our study highlighted selected aspects of expression and functions of non classical HLA class I-like molecules HLA-E, and EPCR, in particular their expression and regulation by human EC, and the mechanisms by which they may have a significant impact on the alloimmune responses to organ transplants. Our data established, for the first time, that HLA-E expression and release of soluble HLA-E are features of EC activation and emphasize immunoregulatory functions of the endothelium (Coupel S. et al., Blood 2007). A collaborative study allows us to demonstrate that in addition to EC, activated melanoma cells also produce soluble HLA-E (Derre L. et al. J. Immunol. 2006), suggesting that soluble HLA-E can be for diagnosis and treatment (INSERM patent, Allard M. et al. PlosONE 2011).The endothelial cell protein C receptor (EPCR) negatively regulates the coagulation and inflammation (Guitton C. et al. , Am. J. Physiol -Cell, 2011) and we identified several factors and mechanisms controlling its expression and release as a soluble factor. We found that gender and EPCR A3 haplotype are major and independent factors affecting sEPCR plasma levels (Guitton et al. J. Vasc. Res. 2011). In patients, severe inflammation, at the onset, only triggers moderate quantitative changes in plasma sEPCR concentration (Guitton C. et al. Int. Care Med. 2011 ). However, an early rise in plasma sEPCR associated with bad outcome and may be use as a surrogate marker.


Notch signaling plays major roles in EC survival, proliferation and transdifferentiation. Since these events are particularly implicated in transplant arteriosclerosis (TA) our recent work aimed to define Notch regulation in graft EC upon inflammation and rejection.  We found a consistent decrease in Notch4 associated with TA in cardiac allografts and in cultured EC in response to proinflammatory cytokines. We demonstrated that silencing Notch4 and hes1 enhances VCAM1 expression, induces apoptosis and impairs endothelial injury repair, suggesting that Notch4 expression is required to maintain EC survival and quiescence (Quillard T. et al. ATVB  2008). We also showed that Notch2 activation in EC promotes caspase-dependent apoptosis. Both forced Notch2NICD expression and Notch2 silencing demonstrate interplay between Notch2 signaling and survivin expression in the control of EC apoptosis. Thus, dysregulated Notch2 signaling by TNF sensitizes vascular endothelial cells to apoptosis and our findings suggest a major role for survivin as effector of Notch signaling (Quillard T., et al. PLos ONE 2009). Finally, our results indicate that TNF elicits a drastic change in the pattern of Notch receptors expressed on vascular ECs. This change corresponds to phenotypic switch where Notch4 is replaced by Notch2 (Quillard T. et al. Biochem. Pharm. 2010). Functionally, activation of Notch2 signaling favors cell death while Notch4 activation was shown to be protective.

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