News Article | May 19, 2017
HEIDELBERG, 19-May-2017 — /EuropaWire/ — The German National Academy of Sciences, Leopoldina, today welcomes EMBO Director Maria Leptin as one of its members. Election to the Leopoldina membership is the highest academic honour awarded by an institution in Germany and it is bestowed on scientists who are experts in their fields. Maria Leptin, together with 14 other eminent researchers from Germany and abroad, was elected in 2016, and will today be officially welcomed at a ceremony in Halle (Saale), Germany. Following the presentation of the membership certificates, Maria Leptin will deliver a lecture on the role of cellular coordination during the development of organs and whole organisms. Through her election, Maria Leptin became part of a membership of over 1,500 individuals from more than 30 countries. Other EMBO Members elected to the Leopoldina Membership in 2016 include Aaron Ciechanover, Haifa, Israel, Veit Hornung, Munich, Germany, Edvard Moser, Trondheim, Norway, May-Britt Moser, Trondheim, Norway, Christian Spahn, Berlin, Germany. For more information (in German): https://www.leopoldina.org/de/presse/pressemitteilungen/pressemitteilung/press/2487/ Maria Leptin received her PhD in 1983 for work on B cell activation carried out at the Basel Institute for Immunology under the supervision of Fritz Melchers. She switched to the study of development in Drosophila when she joined the laboratory of Michael Wilcox at the Medical Research Council’s Laboratory of Molecular Biology (LMB) in Cambridge, UK, for her postdoctoral work on Drosophila integrins. After a research visit at the lab of Pat O’Farrell at the University of California San Francisco (UCSF), where she began studying gastrulation, she spent the years from 1989 to 1994 as a group leader at the Max Planck Institute in Tübingen. In 1994, she became Professor at the Institute of Genetics University of Cologne. In January 2010 Maria Leptin became the Director of EMBO and established a research group in Heidelberg at the European Molecular Biology Laboratory (EMBL). The group studies the development of complex cell shapes in the respiratory system of Drosophila and the role of RNA localisation in generating cell shape. Professor Leptin is an elected member of EMBO, the Academia Europaea and the German National Academy of Sciences (Leopoldina). She also serves on the editorial boards of Developmental Cell, Developmental Biology and on advisory boards of several academic institutions.
Salomonsen J.,Basel Institute for Immunology |
Salomonsen J.,Copenhagen University |
Chattaway J.A.,University of Cambridge |
Chan A.C.Y.,University of Cambridge |
And 34 more authors.
PLoS Genetics | Year: 2014
Many genes important in immunity are found as multigene families. The butyrophilin genes are members of the B7 family, playing diverse roles in co-regulation and perhaps in antigen presentation. In humans, a fixed number of butyrophilin genes are found in and around the major histocompatibility complex (MHC), and show striking association with particular autoimmune diseases. In chickens, BG genes encode homologues with somewhat different domain organisation. Only a few BG genes have been characterised, one involved in actin-myosin interaction in the intestinal brush border, and another implicated in resistance to viral diseases. We characterise all BG genes in B12 chickens, finding a multigene family organised as tandem repeats in the BG region outside the MHC, a single gene in the MHC (the BF-BL region), and another single gene on a different chromosome. There is a precise cell and tissue expression for each gene, but overall there are two kinds, those expressed by haemopoietic cells and those expressed in tissues (presumably non-haemopoietic cells), correlating with two different kinds of promoters and 5′ untranslated regions (5′UTR). However, the multigene family in the BG region contains many hybrid genes, suggesting recombination and/or deletion as major evolutionary forces. We identify BG genes in the chicken whole genome shotgun sequence, as well as by comparison to other haplotypes by fibre fluorescence in situ hybridisation, confirming dynamic expansion and contraction within the BG region. Thus, the BG genes in chickens are undergoing much more rapid evolution compared to their homologues in mammals, for reasons yet to be understood. © 2014 Salomonsen et al.
PubMed | University of Turku and Basel Institute for Immunology
Type: Journal Article | Journal: Immunology today | Year: 2014
Several alternative reasons have been offered for the immunological inertia between the pregnant mother and her fetus. None of these alone has proved correct and sufficient. In this review Paavo Toivanen and Christer Granberg look at one interesting mechanism - the inhibition of maternal lymphocyte reactivity by fetal suppressor cells observedin vitro when untreated populations of maternal and neonatal lymphocytes are cultured together.
Chappell P.,University of Oxford |
Meziane E.K.,University of Cambridge |
Harrison M.,University of Cambridge |
Magiera L.,University of Cambridge |
And 19 more authors.
eLife | Year: 2015
Highly polymorphic MHC molecules are at the heart of adaptive immune responses, playing crucial roles in many kinds of disease and in vaccination. We report that breadth of peptide presentation and level of cell surface expression of class I molecules are inversely correlated in both chickens and humans. This relationship correlates with protective responses against infectious pathogens including Marek's disease virus leading to lethal tumours in chickens and HIV infection progressing to AIDS in humans. We propose that differences in peptide binding repertoire define two groups of MHC class I molecules strategically evolved as generalists and specialists for different modes of pathogen resistance. We suggest that differences in cell surface expression level ensure the development of optimal peripheral T cell responses. The inverse relationship of peptide repertoire and expression is evidently a fundamental property of MHC molecules, with ramifications extending beyond immunology and medicine to evolutionary biology and conservation. © Copyright Sanchez Alvarado.
Ren Q.,University of Kentucky |
Wimmer C.,Basel Institute for Immunology |
Wimmer C.,European Commission |
Chicka M.C.,University of Kentucky |
And 4 more authors.
Blood | Year: 2010
Activation-dependent platelet granule release is mediated by integral membrane proteins called soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptors (SNAREs) and their regulators; however, the mechanisms for this process are ill-defined. To further characterize platelet secretion, we analyzed the function of platelets from Unc13dJinx mice. Platelets from these animals lack the putative vesicle priming factor, Munc13-4, and have a severe secretion defect. Release from dense granules was completely ablated and that from α-granules and lysosomes was severely compromised. Unc13dJinx platelets showed attenuated aggregation and, consequently, Unc13dJinx mice had prolonged tail-bleeding times. The secretion defect was not due to altered expression of SNAREs or SNARE regulators, defective granule biogenesis, or faulty platelet activation. The defective release could be rescued by adding recombinant Munc13-4 to permeabilized Unc13dJinx platelets. In wild-type mouse platelets, Munc13-4 levels were lower than those of SNAREs suggesting that Munc13-4 could be a limiting component of the platelets' secretory machinery. Consistently, Munc13-4 levels directly correlated with the extent of granule release from permeabilized platelets and from intact, heterozygous Unc13dJinx platelets. These data highlight the importance of Munc13-4 in platelets and indicate that it is a limiting factor required for platelet secretion andhemostasis. © 2010 by The American Society of Hematology.
Nutt S.L.,Research Institute of Molecular Pathology |
Nutt S.L.,Wellcome CRC Institute |
Heavey B.,Research Institute of Molecular Pathology |
Rolink A.G.,Basel Institute for Immunology |
Busslinger M.,Research Institute of Molecular Pathology
Journal of Immunology | Year: 2015
The Pax5 gene encoding the B-cell-specific activator protein (BSAP) is expressed within the haematopoietic system exclusively in the B-lymphoid lineage, where it is required in vivo for progression beyond the pro-B-cell stage. However, Pax5 is not essential for in vitro propagation of pro-B cells in the presence of interleukin-7 and stromal cells. Here we show that pro-B cells lacking Pax5 are also incapable of in vitro B-cell differentiation unless Pax5 expression is restored by retroviral transduction. Pax5-/-pro-B cells are not restricted in their lineage fate, as stimulation with appropriate cytokines induces them to differentiate into functional macrophages, osteoclasts, dendritic cells, granulocytes and natural killer cells. As expected for a clonogenic haematopoietic progenitor with lymphomyeloid developmental potential, the Pax5-/-pro-B cell expresses genes of different lineage-affiliated programmes, and restoration of Pax5 activity represses this lineage-promiscuous transcription. Pax5 therefore plays an essential role in B-lineage commitment by suppressing alternative lineage choices. © 1999 Macmillan Magazines Ltd.
PubMed | Basel Institute for Immunology
Type: Journal Article | Journal: Immunogenetics | Year: 2011
The unresponsiveness to LPS detected in C57BL/10Cr mice is inherited as a recessive trait and is determined by an autosomal gene linked to theMup-1 locus on chromosome 4. Since no complementation for LPS responsiveness was observed in F(1) hybrid mice between C3H/HeJ and C57BL/10Cr, we conclude that C57BL/10Cr mice carry a defective allele at the sameLps locus, previously identified by the mutation detected in the C3H/HeJ strain.