Name : REYNAUD
First name: Claude-Agnès
Date and place of birth: 6th of march, 1953 at Paris (France)
Single, two children
Present activity : INSERM U1151/CNRS UMR8253 Institut Necker-Enfants Malades (INEM) - Team « Développement dui système immunitaire » - Université Paris Descartes, Faculté de Médecine – Site Broussais – CS61431 - 14 rue Maria Helena Vieira Da Silva – 75993 PARIS CEDEX 14 (France)
email@example.com, 00 33 1 72 60 64 48
Field of expertise : immunology, B cell development, mechanisms of formation of the immunoglobulin repertoire, B cell memory, DNA polymerases, DNA repair and mutagenesis.
- june 1972 : Ecole Normale Supérieure (option Physical Sciences)
- 22 mai 1981 : PhD thesis (University Paris 7)
- September 1974-May 1981 : PhD student at Institut Jacques Monod (Paris) (director of thesis : Klaus Scherrer)
- June 1981-October 1987 : Research assistant, Institut Jacques Monod (Paris) (Head of group: Jean-Claude Weill)
- November 1987-December 1991 : member of the Basel Institute for Immunology (Basel, Switzerland)
- since January 1992: Director of Research (CNRS), INSERM U373 "Développement du Système Immunitaire" (Faculté de Médecine Necker Enfants-Malades – Paris) (head of group: Jean-Claude Weill 1992-1996, Harald von Boehmer 1997-1999)
- october 2000: DR1 C.N.R.S
- since January 2001: head of INSERM U373 (now U783)
Selected adminstrative responsabilities
Member of committee « biologie-santé » of the ANR blanc program (2005-2007)
AERES Scientific delegate for Immunology 2009-2010
Member of the EMBO longterm fellowship committee (2008-2013)
Member of the scientific committee of the Ligue Nationale contre le Cancer
Director of the Structure Fédérative de Recherche (SFR) Necker
- Prix "jeune chercheur", Fondation pour la Recherche Médicale (1987) - mention "Immunologie".
- Médaille d'Argent du CNRS, 1991.
- Prix Jean-Pierre Lecocq of the Académie des Sciences de Paris (1997), together with Jean-Claude Weill.
- EMBO member (2000)
- Honorary member of the American Association of Immunologists (2005)
Molecular and cellular strategies of development and diversification of B lymphocyte subsets
Our lab has a long-lasting interest in the molecular and cellular mechanisms involved in the development and diversification of the B cell repertoire. These approaches, initially focused on species like birds and ruminants in the 80-90s, have uncovered an unsuspected diversity in the modes of repertoire formation, involving mechanisms like gene conversion and somatic mutation in the formation of the pre-immune repertoire in these species.
More recently our approaches have focused, on the molecular side, on the contribution of non-replicative DNA polymerases to the process of V(D)J recombination and somatic hypermutation: this involved the identification of two new polymerases, Pol mu and Pol lambda, and their contribution to the non-homologous end joining process occurring during the assembly of a complete immunoglobulin gene; for the hypermutation process taking place during immune responses, this involved the identification of the key role played by DNA polymerase eta, and the striking back-up achieved by enzymes of the same family upon its inactivation, both in humans and in mice.
On the cellular side, we have characterized marginal zone B cells in humans as a specific subset susceptible of repertoire diversification outside T-dependent and independent responses, as well as their distinct differentiation and survival requirements. We have also developed a new mouse reporter line allowing the follow-up of B cell memory subsets generated during an immune response, and identified multiple layers of B cell memory with distinct functional characteristics: an "effector memory" subset endowed with the capacity to rapidly expand and differentiate into immunoglobulin secreting cells, and a "central memory" subset capable of re-initiating a germinal center response.
Our present interests focus on investigating the discrepancies observed between mouse models of immune responses and observations performed in humans, with the aim of understanding the relative contribution of intrinsic, species-specific developmental differences vs. the impact of the radically different experience of the outside infectious world that laboratory mice and human beings undergo.