BioNTech AG, Tron Translationale Onkologie An Der Universitatsmedizin Der Johannes Gutenbe and Johannes Gutenberg University Mainz | Date: 2015-05-07
The present invention relates to expressing RNA in cells and, in particular, enhancing viability of cells in which RNA is to be expressed. Specifically, the present invention provides methods for expressing RNA in cells comprising the steps of preventing engagement of IFN receptor by extracellular IFN and inhibiting intracellular IFN signalling in the cells. Thus, preventing engagement of IFN receptor by extracellular IFN and inhibiting intracellular IFN signalling in the cells allows repetitive transfer of RNA into the cells.
BioNTech AG | Date: 2015-07-10
The invention relates to the identification of genetic products that are expressed in association with a tumor and the nucleic acid coding therefor. The invention relates to the therapy and diagnosis of diseases in which the genetic products that are expressed in association with a tumor are expressed in an aberrant manner. The invention also relates to proteins, polypeptides, and peptides which are expressed in association with a tumor and the nucleic acids coding therefor.
BioNTech AG and Johannes Gutenberg University Mainz | Date: 2015-11-05
The present invention provides methods for de-differentiating somatic cells into stem-like cells without generating embryos or fetuses. More specifically, the present invention provides methods for effecting the de-differentiation of somatic cells to cells having stem cell characteristics, in particular pluripotency, by introducing RNA encoding factors inducing the de-differentiation of somatic cells into the somatic cells and culturing the somatic cells allowing the cells to de-differentiate.
BioNTech AG and Johannes Gutenberg University Mainz | Date: 2014-12-16
The present invention provides recombinant proteins comprising the amino acid sequence of an intracellular segment of CD40 and an amino acid sequence mediating the association of the recombinant protein with the constant region of an immunoglobulin heavy chain. The recombinant proteins according to the present invention are useful for inducing clonal expansion of a B cell having a predetermined antigen-specificity without the need for T cell or CD40L mediated co-stimulation. Thus, the present invention provides tools for clonal expansion of B cells specific for an antigen of interest and the production of B cells secreting antibodies specific for an antigen of interest. The recombinant proteins of the present invention may also be used for generating fully human monoclonal antibodies with a predetermined antigen-specificity from the B cell repertoire of a human subject.
Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-2012-ITN | Award Amount: 3.54M | Year: 2013
Neuroinflammatory disease, in particular multiple sclerosis affects more than 700.000 people within Europe alone. European countries are at the forefront of neuroimmunological research and students in medicine and biology are greatly attracted by the field. Neuroimmunology research further impacts our understanding of the ethiopathology of other CNS-disorders including Alzheimers Dementia and Morbus Parkinson. The ability of inflammatory immune cells to cause tissue damage within the nervous system is largely governed by soluble mediators including cytokines/chemokines, cytolytic molecules and growth factors. The therapeutic targeting of such mediators has proven successful for the treatment of a number of inflammatory diseases, yet is failing for the treatment of neuroinflammatory disorders. Clearly, the rules and regulatory elements, which govern inflammation and tissue injury within the CNS, differ significantly from those of other tissues and a unique CNS-focused research approach to unravel these rules is required. In this ITN proposal, we will train ESRs and ERs specifically in Neuroimmunology by combining prominent laboratories in academia and industry on the task to study the communication networks between immune and CNS-resident cells. Scientifically, we focus particularly on the soluble factors mediating cell-cell communication at the immune-CNS interface. To this end, we combine expertise in molecular and cellular Neuroimmunology with Neuropathology of human and animal models of CNS inflammation. In addition, our goal is to further utilize inflammatory processes for neuroprotection.