Nuala Mooney
  • E-mail :[email]
  • Phone : + 33 1 42 49 95 51
  • Location : Paris, France
Last update 2012-01-30 17:24:32.079

Nuala Mooney Ph D Pathology

Course and current status

Ph D University of London 1984 (Pathology)

B.Sc.Hons University of Bath 1978 (Biochemistry)

 

Team leader 'Regulation of the immune response by the antigen presenting cell' INSERM UMR_S 940

Director of research (CNRS) 1998

Assistant professor  (CNRS) 1991

Medical research council/INSERM post-doctoral fellow 1988-1990

Scientific summary

Team “Regulation of the immune response by the antigen presenting cell” Nuala Mooney

The major obstacle to organ transplantation is the generation of an alloimmune response principally mediated by MHC molecules present on donor cells. While professional MHC class II expressing antigen presenting cells ( eg dendritic cells) control the adaptive CD4+-T cell response under physiological conditions, the inflammation generated by transplantation leads to activation and increased MHC class II expression by non-professional antigen presenting cells including endothelial cells. We have experience in the mechanisms of regulation of antigen presentation in dendritic cells and in B lymphocytes (Sloma et al J of Immunol 2008, Delaguillaumie et al Eur J Imm 2008). However the antigen presenting capacity of the endothelial cell (EC) remains to be fully characterized and particularly because endothelial cells of different vascular origin have different abilities to generate an alloimmune response. We have shown that microvascular HLA-class II+ endothelial cells can regulate the local inflammatory allogeneic response by promoting either an IL-6/STAT-3 dependent Th17 response or a contact-CD54 dependent regulatory response according to the cytokine environment (Taflin et al., PNAS 2011). However, human endothelial cells are also targets of allograft recipient HLA class I and class II antibodies directed against donor cells. Our project addresses the mechanisms by which the endothelial cell acts as both a target and as an initiator of the alloresponse under inflammatory conditions and the regulation of these roles.

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