Scientific Aim

The Landsteiner Foundation for Blood Transfusion Research (LSBR) supports fundamental research, including clinical and experimental investigations, in the field of blood, blood derivatives, and blood (related) diseases, provided that these topics are related to transfusion or blood cell transplantation.

This scope spans a wide range of subjects in the field of hematology, including haematopoiesis, haemostasis, immunotherapy, transfusion medicine, and other issues relevant to the field.

Pre-applications 2023

Submission for Pre-Applications for Scientific Research 2023 is closed.

In 2023 the LSBR grants for research projects have a maximum of 450,000 Euro and the fellowship project will have a maximum of 700,000 Euro (project for 5 years).
See also on the page: Information for the applicant.

Granted in 2022

A grant is only awarded when the applicant has received written confirmation signed by the chair and the director of the LSBR.

2202 – Monika Wolkers – Hemostopoiesis – Sanquin Research
How translation regulation defines T-cell function in health and disease.
T cells are critical to clear our body from pathogens and malignant cells. However, T cells gradually become dysfunctional in chronic infections and in tumors and lose their capacity to produce effector molecules. Features of dysfunctional T cells are measured by mRNA expression. We however previously showed that mRNA expression levels poorly represent the actual expression of the respective protein, which in particular holds true for T cell effector molecules. Here, we will decipher which parameters determine this discrepancy between mRNA and protein expression. We will first identify the proteins that depend this translation regulation. we will then identify the sequences within the mRNA that regulate the translation into proteins. Lastly, we validate the role of the identified sequences in specific transcripts of T cells. Identifying how protein production in T cells is regulated in health and disease will not only yield novel fundamental insights in T cell biology. It will also provide new angles to regulate gene expression in T cells and thus improve their anti-tumoral function, a critical feature for improving T cell products for the clinic.

2208 – Ruben van Boxtel / Inge van der Werf – Prinses Máxima Center for Pediatric Oncology – Utrecht
Characterizing early life hematopoiesis: why does bone marrow sometimes fail?
Hematopoiesis ensures a balanced production of all blood cells throughout life. Yet, already early in life, our bone marrow (BM) can fail and stop producing new blood cells. When BM failure happens, it is important to differentiate between a malignant (i.e., cancerous) and benign origin for proving the correct treatment. However, this can be challenging as few cells are present in the bone marrow due to the disease. Also, we do not really know why the bone marrow fails so early in life. We aim to identify these causes by studying individual cells in the failing bone marrow, bypassing the problem that only few cells are present in these children. In our lab, we are specialized in studying blood at single cell level and have already obtained unique knowledge of healthy bone marrow in children. By comparing this knowledge with the results of this proposed study, we will be able to study why bone marrow can fail early in life. We envision that this knowledge will improve diagnostics, facilitate choice of treatment, and perhaps even contribute to developing strategies to prevent bone marrow failure in children.

2115 – FELLOWSHIP – Anna Marneth – Hematology – Radboud University Medical Center (Nominator: Joop Jansen)
The role of C-mannosylation in MPL function and megakaryopoiesis.
Blood platelets are small cell particles that are essential for blood clotting and hence prevent excessive bleedings. Patients with a defect in platelet formation suffer from bleedings. Vice versa, patients with elevated platelets are at risk for blood clotting that could block blood supply to major organs. These serious health problems underscore the importance of balanced platelet formation. One crucial protein that regulates the growth of platelet-producing cells and platelet levels is MPL. My preliminary data strongly suggests an essential role for the sugar modification “C-mannosylation” in MPL function. I propose to decipher how C-mannosylation influences MPL function and platelet production. Additionally, I will uncover C-mannosylation disturbances in patients with too few or too many platelets. Knowledge on this vastly unexplored topic can then be exploited for therapeutic purposes and to improve in vitro platelet production for transfusions.

2217 – FELLOWSHIP – Bart Weijts – Dr. Robin Laboratory – Hubrecht Institute (Nominator: Catherine Robin)
Phenotypical characterization of an endothelial derived macrophage population that resides in the blood vessels.
Macrophages provide the first line of defence against pathogens and can be found in virtually all tissues and organs of the body, except in blood vessels. These vessels must thus be protected from injury and pathogens by other cells, still unidentified. In this project, we aim to characterize a novel population of macrophages that we found in the blood vessels and are atypically produced by endothelial cells forming the vessel walls, hence we termed them endothelial macrophages (eMΦ). Our preliminary data suggests that eMΦ phagocytose bacterial particles and dying or faulty cells in the blood. Characterizing eMΦ and their precise role in physiological and non-physiological conditions will provide novel insights into the protection mechanisms of blood vessels and blood. Tailoring eMΦ to combat pathogens or cancerous cells present in the blood could be part of future immunotherapy strategies.

2220 – Maartje van den Biggelaar / Suzanne Fustolo-Gunnink – Neonatal Clinical Transfusion Research group and Proteomics – Sanquin Research
Translational epidemiology to optimize neonatal platelet transfusions.
Background: babies born prematurely often receive transfusions with blood platelets when their blood platelet count is low. The aim of these transfusions is to prevent bleeding. A recent study unexpectedly showed that when transfusions are given at a higher platelet count of 50, more babies develop severe bleeding or die than if we wait until the platelet count is 25. This means that platelet transfusions can cause harm in premature babies. The mechanism for this harm is unknown.
Aim: the aim of this study is to understand how platelet transfusions cause harm in premature babies.
Method: with a team of doctors, laboratory researchers and epidemiologists, we will collect blood samples at regular time points from babies born before 30 weeks of pregnancy who were admitted to Dutch intensive care units for babies. We will also collect their platelet counts, information about bleeding and transfusion products, and important data regarding their health. We will analyze the samples using proteomics, a technique which allows us to measure all the proteins present in their blood. Proteins are the building blocks of the human body, and changes in the concentration of proteins can tell us which systems of the body are being activated or deactivated. The combination of the protein patterns and data on transfusions and bleeding can help us understand how platelet transfusions can cause harm.
Impact: this study will help doctors to understand how platelet transfusions can cause harm in premature babies. Ultimately, we can prevent bleeding and even safe lives by making sure that doctors transfuse only those babies who have the highest chance of benefitting from the transfusion.

History

In 1948 the Dutch government, the Dutch Red Cross and the municipality of Amsterdam founded the Central Laboratory of the Blood Transfusion Service of the Netherlands Red Cross (CLB) and installed its supporting foundation the Stichting tot Instandhouding van het CLB (StICLB). For 50 years this foundation supported the activities of CLB, including research in the field of blood transfusion and the manufacturing of plasma products. Its board acted as the supervisory board of CLB.

In 1998 CLB merged with the 22 Dutch regional blood banks into a new foundation, i.e. Sanquin Blood Supply Foundation. The merger did not include StICLB, which needed to adapt its statutes to ensure that the (financial) assets of StICLB remained available for continued support of the research in the field of blood and blood transfusion in The Netherlands. The name of StICLB was changed to Landsteiner Stichting voor Bloedtransfusieresearch (LSBR). The LSBR is an independent foundation that uses the revenues of its assets to support research proposals from Sanquin and other Dutch institutes in the same field.

Article 3 of the LSBR statutes of 17 April 2015 specifies the objectives of LSBR:

• to support scientific research, especially basic research, in blood transfusion and related subjects
• to fulfill moral and social obligations, especially obligations originating from the history of the foundation
• to manage the financial assets of the foundation.