Bio

Professional Education


  • Licence, Universite Paul Sabatier (2007)
  • Maitrise, Universite Paul Sabatier (2008)
  • Master of Science, Universite Paul Sabatier (2009)
  • Doctor of Philosophy, Universite Paul Sabatier (2013)

Stanford Advisors


Publications

Journal Articles


  • Defects of filaggrin-like proteins in both lesional and nonlesional atopic skin JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY Pellerin, L., Henry, J., Hsu, C., Balica, S., Jean-Decoster, C., Mechin, M., Hansmann, B., Rodriguez, E., Weindinger, S., Schmitt, A., Serre, G., Paul, C., Simon, M. 2013; 131 (4): 1094-1102

    Abstract

    Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a disturbed epidermal barrier. In a subset of patients, this is explained by nonsense mutations in the gene encoding filaggrin (FLG).We sought to evaluate the respective role of FLG mutations and proinflammatory cytokines and to assess the expression of FLG, hornerin (HRNR), and FLG2, 2 FLG-like proteins, which are involved in epidermal barrier functions, in normal skin and both lesional and nonlesional skin of patients with AD.An FLG-genotyped cohort of 73 adults with AD and 73 aged-matched control subjects was analyzed by using immunohistochemistry and immunoblotting. Normal primary human keratinocytes were differentiated in either the absence or presence of IL-4, IL-13, and IL-25.Compared with control subjects, FLG, HRNR, and FLG2 were detected at significantly lower levels in the skin of patients with AD, irrespective of their FLG genotype. The reduction was greater in lesional compared with nonlesional skin. In addition, the proFLG/FLG ratio was found to be higher in the skin of wild-type patients than in control subjects. Cytokine treatment of keratinocytes induced a dramatic reduction in FLG, FLG2, and HRNR expression both at the mRNA and protein levels.The stratum corneum of lesional but also clinically unaffected skin of adults with AD is abnormal, with reduced expression of FLG and FLG-like proteins. In addition to nonsense mutations, proinflammatory cytokines and some defects in the proFLG processing can contribute to the FLG downregulation. Our study suggests that skin inflammation reduces the expression of FLG-like proteins, contributing to the AD-related epidermal barrier dysfunction.

    View details for DOI 10.1016/j.jaci.2012.12.1566

    View details for Web of Science ID 000317187200019

    View details for PubMedID 23403047

  • Update on the epidermal differentiation complex FRONTIERS IN BIOSCIENCE-LANDMARK Henry, J., Toulza, E., Hsu, C., Pellerin, L., Balica, S., Mazereeuw-Hautier, J., Paul, C., Serre, G., Jonca, N., Simon, M. 2012; 17: 1517-1532

    Abstract

    On human chromosome 1q21, a 2-Mb region called the epidermal differentiation complex comprises many genes encoding structural and regulatory proteins that are of crucial importance for keratinocyte differentiation and stratum corneum properties. Apart from those for involucrin and loricrin, most of the genes are organized in four families: the genes encoding EF-hand calcium-binding proteins of the S100A family, the genes encoding the small proline rich proteins (SPRRs) and the late cornified envelope (LCE) proteins, two families of cornified cell envelope components, and the genes encoding the S100-fused type proteins (SFTPs). This review focuses on the SPRRs, LCE proteins and SFTPs. It describes their structures, their specific functions and, when known, the mechanisms involved in the regulation of their expression. It also highlights their possible involvement in skin diseases.

    View details for DOI 10.2741/4001

    View details for Web of Science ID 000300053700021

    View details for PubMedID 22201818

Stanford Medicine Resources: