September 2017
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Vendredi Amphi Pasteur - Tour Inserm CERVI * |
« Regulation of T cell responses by distinct forms of autophagy » | |
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Fernando MACIAN JUAN (Albert Einstein College of Medicine Dpt of Pathology and Institute for Aging Research Bronx – NY – USA ) contact: mathias.faure@inserm.fr Fernando MACIAN JUAN has more than 20 years of experience in the study and characterization of the molecular mechanisms that regulate T cell activation and tolerance. His group has pioneered the identification and characterization of the signaling pathways, transcriptional complexes and molecular events that regulate the functional outcome following T cell receptor engagement in peripheral T cells. His studies have contributed to the identification of the transcriptional and signaling events that regulate T cell fate upon antigen encounter and determine T helper cell differentiation, activation and tolerance. In the last 10 years, his group has helped defined the roles and regulation of different forms of autophagy in T cell biology and has contributed to the establishment of autophagy as an essential cell process in the modulation of T helper cell responses.
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Mardi Amphi Pasteur - Tour Inserm CERVI * |
« Oxygen interplay during Shigella infection » | |
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Benoit MARTEYN (Institut Pasteur de Paris, Unité de Pathogénie Microbienne Moléculaire, Gustave Roussy Cancer Campus) Contact : thomas.henry@inserm.fr Shigella is a pathogenic enterobacteria which is the causative agent of the bacillary dysentery or shigellosis. Until now, no vaccine against Shigella is commercialized. Tremendous efforts have been made to to better understand the modulation of Shigella virulence step in vivo. Shigella expresses three different secretion systems, T3SS, T5SS and T6SS, whom role is studied during the infectious process. In particular, we investigate to which extent oxygen is required for Shigella virulence activation (mediated |
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Lundi Salle des Thèses Chantal Rabourdin-Combe |
« Beyond networks: dynamic mechanisms for developmental processes » | |
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Johannes JAEGER (Konrad Lorenz Institute, Vienna) |
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Mardi Sous-sol LR5 |
« Role of retroviral receptors in phosphate homeostasis and calcification » | |
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Jean-Luc BATTINI (Institut de Recherche en infectiologie de Montpellier -IRIM- CNRS UMR 9004 - Université de Montpellier) Contact : flcosset@ens-lyon.fr Phosphate is one of the key minerals in the body that participates in the synthesis of nucleic acids and membranes, bone and tooth mineralization, energy production (ATP) and signal transduction. At the same time, phosphate can be toxic when it exists in excess. Phosphate is present in blood, cerebrospinal fluid (CSF) and cells and its concentration is tightly regulated by phosphate transporters. Defect in phosphate transport may thus have severe clinical consequences. We are interested in a family of retroviral receptors that transport phosphate and that were recently associated to a familial brain calcification disease. Recent avances on the role of these retroviral receptors/phosphate transporters in phosphate homeostasis and sensing will be presented. Legati A., Giovannini D., …, Geschwind DH., Battini JL.*, Coppola G*. 2015. Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export. Nature Genetics 47: 579–581. |
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Cécile MARTINAT (ISTEM) Hôte : Hélène Polvèche |
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Mercredi Amphi Pasteur - Tour Inserm CERVI * |
« Disabling of T-lymphocyte immune response by Ebola Virus » | |
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Mathieu LAMPIETRO (University of Texas Medical Branch, Galveston National Laboratory – USA) Contact : branka.horvat@inserm.fr Ebola Virus Disease (EVD) is characterized by a rapid evolution leading to a sepsis-like syndrome that is associated with low counts of immune cells and particularly lymphopenia, which is uniformly observed in all fatal cases. Nonetheless, the mechanisms by which EBOV rapidly overpowers the host’s immune responses remain largely unknown. In our studies, we demonstrated that despite an absence of productive infection, Ebola virus directly binds to T-lymphocytes. We show that membrane bound virions are rapidly internalized and co-localize with endosomal markers. Specifically, Ebola glycoprotein (GP) interaction with TLR4 and/or viral membrane associated phosphatidylserine (PS) with Tim-1 on the surface of T-cells result in increased cytokine production consistent with non-specific activation and an overall contribution to the onset of a cytokine storm. Overall, these interactions resulted in a significant increase in cell death, which may contribute to the lymphopenia observed in vivo. |
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Amphi SVT |
«Integrating cell signaling and cell biomechanics in development: the case of teeth » | |
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Isaac SALAZAR CIUDAD (University of Helsinki, Biotechnology Institute) contact : Nicolas Goudemand
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« Chromatin dynamics at nano-scale resolution and long-range correlation within the nucleus during transcription » | |
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Haitham Ahmed SHABAN (LBME/CBI-CNRS; University of Toulouse) Hôte : Cedric Vaillant & Geneviève Fourel Intrinsic high dynamics of chromatin is an essential underpinning of gene regulation. Control of gene expression largely occurs at the transcription stage and involves modifications of chromatin structure and transcription factors binding along with RNA polymerase II dynamics. However, it remains unclear how global and local motion of chromatin interleaves with the choreography of other transcription players. And also, how chromatin clusters respond dynamically through coordinate movements to regulate genomic processes.For this purpose, we developed a method to estimate motion at sub-pixel resolution with high accuracy over the entire nucleus in live human cells. Although the fluorescence intensity of chromatin images is diffraction-limited, our method reveals sub-diffraction vectorial information based on reconstructed dense global flow fields of fluorescent images. This approach allows us parallel quantification of key biophysical properties (such as diffusion coefficient and the underlying modes of motion) of distinct labeled entities in one single cell: H2B-GFP and SiR- Hoechst as chromatin and DNA markers, in human cultured cells. We were thereby able to study nucleus-wide chromatin motion in healthy culture cells, or upon treatment with drugs that inhibits transcription at distinct stages (initiation or elongation), or upon serum deprivation which is also known to globally affect transcription.Our method points first to a major heterogeneity in chromatin motion over the entire nucleus, whatever transcription state. This heterogeneity strongly suggests that nucleosome clustering (density & dynamics within clusters) along chromatin fibers is itself highly heterogeneous.We observed a striking correlation in transcriptional state between chromatin areas that display coherent motions over the entire nucleus. We further observed that coordinated movements within domains differentially correlate with RNA pol II activity. Similar trends with regard to transcriptional state were observed for global spatial correlation of chromatin dynamics upon pausing transcription at initiation, whereas correlation was significantly altered when elongation was halted. Finally, quantification of spatial smoothness in nuclear space over large time intervals points to clear-cut boundaries between distinct motion modes, while smooth transitioning in a small neighborhood instead dominate for short time intervals. |
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Mardi Amphi Pasteur - Tour Inserm CERVI * |
« In vivo manipulation of T cell fate in skin immunity » | |
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Iris GRATZ (University of Salzburg – Austria) Contact : pia.gamradt@inserm.fr The principal goal of Iris Gratz' research is to investigate thmechanisms of immune regulation in the skin. During her first Postdoc at the University Hospital Salzburg, Austria, she developed approaches to induce antigen-specific immune tolerance to skin antigens. During her second Postdoc with Professor Abul Abbas at the University of California, San Francisco, she then established novel mouse models to study T cell mediated immune responses and regulatory processes in the skin. She
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Mardi Amphi Pasteur - Tour Inserm CERVI * |
« From epithelial dysregulation to atopy – Are we allergic to cancer ? » | |
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Jessica STRID ( Senior Lecturer, Imperial College London) Contact : pia.gamradt@inserm.fr Dr Jessica Strid is a Non-clinical Senior Lecturer at the Department of Medicine, Division of immunology and inflammation, Imperial College London. Dr Strid did her MSc degree at the Danish University of Pharmaceutical Sciences in Copenhagen. She did her PhD in immunology at the Institute of Child Health, University College London, UK with a focus on food allergy and skin immunology. As a PostDoc she joined Adrian Hayday's research group at Kings College London and later worked at Cancer Research UK. Her PostDoc studies were focused on autologous 'sterile' stress responses in the skin and their recognition by resident immune cells. In July 2012 Dr Strid joined Imperial College London as a Non-clinical Lecturer and the following year was awarded the Wellcome Trust New Investigator Award. Her current work focuses on tissue immune surveillance and the role of type 2 immunity. The current lecture will discuss the capacity of tissue resident lymphoid cells to directly sense epithelial cell stress and initiate a restorative response. It will explore the type 2 nature of this response and particularly its links to type 2 B cell biology and induction of IgE antibodies. A role for IgE as a host defense mechanism against environmental DNA-damaging xenobiotics and a cooperative role for T and B cell immune surveillance in epithelial tissues will be Proposed |
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Mercredi Salle des Thèses Chantal Rabourdin-Combe |
«Tracing the Evolution of Bacterial Pathogens, from Paleozoic Origins to the Hospital » | |
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François LEBRETON (Massachusetts Eye and Ear infirmary, Boston– USA) Contact : thomas.henry@inserm.fr françois.vandenesch@inserm.fr Why, among the vast diversity of gut flora, enterococci are so well adapted to the modern hospital environment. Molecular clock estimation, together with analysis of their environmental distribution, phenotypic diversity and concordance with host fossil records, place the origins of the enterococci around the time of animal terrestrialization – 425 - 500 MYA. Speciation appears to parallel the diversification of hosts, including the rapid emergence of new enterococcal species following the End Permian Extinction. Major drivers of speciation include changing carbohydrate availability in the host gut. Life on land would have selected for the precise traits that now allow pathogenic enterococci to survive desiccation, starvation, disinfection and antibiotic treatments in the modern hospital; foreordaining the emergence of MDR lineages as leading hospital pathogens. |
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