Bernard Malissen - Biography#

Bernard Malissen is Emeritus CNRS Research Director at Centre d'Immunologie de Marseille Luminy (CIML, Marseille, France) and Centre for Immunophenomics (CIPHE, Marseille, France). He received his PhD training in Immunology at CIML during which he succeeded expanding and characterizing functional human T cell clones and elucidating together with Bertrand Jordan and Marie Malissen the first genomic sequence of a human class I major histocompatibility (MHC) molecules. He then spent two years as a Visiting Associate in the laboratory of Leroy Hood at the California Institute of Technology (Caltech) where he developed gene-transfer approaches to analyze the function of MHC molecules. In 1984, he became a team leader at CIML and directed CIML from 1995 to 2005. After his return to France, he succeeded reconstructing a full T cell antigen receptor (TCR) complex and demonstrated that the present-day signaling subunits associated with antigen receptors stem from a common primordial building block. In collaboration with Marie Malissen, he provided the first evidence for chromosomal inversion during TCR gene rearrangements. In collaboration with the team of J-C Fontecilla-Camps, he elucidated the first atomic structure of several alloreactive TCR in complex with their peptide-MHC ligands, providing a molecular explanation for the basis of transplant rejection and TCR binding-degeneracy. The need to perform functional genomics via massive edition of the mouse genome led him to found CIPHE in 2012, allowing his team to develop large series of innovative mouse models allowing to tackle the function of T cells, dendritic cells and macrophages in their physiological context. More recently, to make sense of the formidable complexity of the signal transduction networks involved in T cell activation, he developed high-throughput “omic” approaches designed to further the understanding of T cell function under normal and pathological conditions. His team recently discovered a novel molecule called Carmil2 and showed that it can be harnessed to induce potent solid tumor-specific T cell responses in the absence of CD28 and of immune checkpoint inhibitors.