The Landsteiner Foundation for Blood Transfusion Research (LSBR) supports clinical and experimental scientific research in the field of blood, blood-forming tissue, blood products, and blood (related) diseases, provided that the research bears a relationship to the field of transfusion or transplantation of blood cells.
The Board of the Landsteiner Foundation for Blood Transfusion Research announces that Pre-Applications for Scientific Research Projects can be submitted.
Standard forms for pre-applications can be downloaded: LSBR pre-application form
The pre-application period closes on 1 February 2020, 23:59 hours. See important dates.
Only one pre-application per applicant will be allowed. Only electronic submission.
LSBR Fellowship 2020
In addition to proposals for project grants, it is also possible to submit proposals for an LSBR fellowship.
NOTE: The LSBR fellowship program of 2020 has been changed compared to 2019.
The LSBR fellowship program, over a period of five years, is intended for talented and creative researchers trying to establish a new research line.
Please find additional information on the download page: Downloads
Please contact the bureau of the LSBR if you intend to write a pre-application for a fellowship grant: Contact
Granted projects 2019
1931 – A.P.J. Vlaar – AMC – Department of Intensive Care Medicine
Transfusion-associated circulatory overload (TACO) – a breathtaking syndrome.
Transfusion-associated circulatory overload (TACO) is the leading cause of transfusion related morbidity and mortality. The underlying mechanism for onset of TACO is unknown. The current proposal aims through a translational approach to understand the mechanisms involved in the onset of TACO and establish a basis to develop preventive and therapeutic strategies for this life-threatening syndrome.
1901 – T. van der Poll – AMC – CEMM
Role of platelet glucose metabolism in hemostasis and inflammation.
Platelets are essential for hemostasis (the process that causes bleeding to stop), but also play an important role in the regulation of inflammatory responses. Low platelet counts can result in bleeding, but this almost exclusively occurs at body sites of inflammation. Platelets need energy for their activation. This project aims to determine how platelets utilize glucose to generate energy and to exert their effects on hemostasis and inflammation. For this we will study glucose metabolism in platelets of patients with systemic inflammation caused by sterile injuries or infection, as well as mice with inflammation and/or infection in which essential mediators of glucose metabolism have been deleted specifically in platelets. Finally, we will study to which extent effective glucose metabolism in platelets contributes to the efficacy of platelet transfusions with regard to control of bleeding.
1908 – G. Vidarsson – Sanquin – Experimental Immunohematology
Mechanistic dissection of clinically relevant allo-antibodies.
Blood transfusion can be a lifesaving intervention. However, it can also result in formation of antibodies, requiring extensive blood matching. Antibodies can also be formed during pregnancies, creating life-threatening conditions for the fetus and newborn. The problem is that identifying patients requiring intervention is currently next to impossible because not all antibodies are apparently created equal. Some antibodies against blood cells have higher destructive potency due to altered sugars in the antibodies, while other antibodies also can recognize other cells, such veins and placenta. Here we will follow up our previous findings of enhanced severity due to altered antibody glycosylation in these diseases, by now also including antibodies specifically recognizing veins, only reacting with platelets, or cross-reacting with both. This will help to make evidence based choices for future diagnostics efforts to identify those at risk and offer them treatment.
1922 – Dr. M.D. Hazenberg – AMC – Hematology
Innate lymphoid cells at the barriers for allogeneic hematopoietic cell transplantation patients.
Transplantation of stem cells derived from a healthy donor is a powerful tool in the treatment of patients with acute leukemias or lymphomas. However, such allogeneic stem cell transplantations are often complicated by donor immune system reactions against healthy tissues of the donor, referred to as graft versus host disease (GvHD). Innate lymphoid cells (ILC) are cells that protect tissues such as the gut epithelium against GvHD. Transplanted patients often have however low numbers of ILC. We will study ways to improve recovery of ILC after allogeneic stem cell transplantation, to prevent the development of GvHD and help protect patients against this often-devastating complication of allogeneic stem cell transplantation.
1923 – M. van den Biggelaar – Sanquin – Laboratory of Proteomics
Cytokine network architecture at the endothelial interface: The whole is greater than the sum of its parts.
Our immune system communicates with the vessel wall by secreting a large variety of soluble chemical messages. These extracellular signals translate into cellular responses that result in the attraction of white blood cells which can subsequently migrate over the vessel wall into the underlying tissues in order to clear infections and dispose of tissue damage. We have recently shown that messages from immune cells of the innate system initiate vastly different processes in the vessel wall compared with messages from immune cells of the adaptive system. In addition, we also showed that combinations of these messages together induce specific responses. However, the diversity and specificity of the vessel wall responses are completely unclear. In this project, we will map >100 inflammatory signatures and link these to immune cell trafficking. This will pave the way for rational design of therapeutic strategies aimed to selectively modulate immune cell trafficking across the vessel wall.
submitted in 2018, granted in 2019
1842 (fellowship) – R. Spaapen – Institute: Sanquin – Immunopathology
Shielding of immune cell receptors by glycosphingolipids
Cells in the body can communicate through protein-protein interactions. This process is essential for immune responses against viruses and cancer, but also in autoimmunity. In my lab, we recently discovered that certain glycolipids on the surface of cells can shield proteins from their communication partners. We showed that this shielding determines the strength of responses by T cells of the immune system. The specific subclass of glycolipids is highly abundant on acute leukemia cells. In this proposal, we will investigate the mechanism behind the interplay between glycolipids and proteins. Furthermore, we will determine the role of leukemia derived glycolipids for the onset and quality of T cell driven immune responses in vivo. I expect to provide novel insights in regulation of anti-tumor T cell responses which may also be relevant to the fields of infection and autoimmunity. Our findings may further provide targets for therapeutic modulation of T cell responses.
Decisions by the Boards of the LSBR (in Dutch) can be found on the page of our Annual Report (in Dutch).