BaHSic — Blood group Antigens, Hematopoiesis and Sickle cell disease
Hematopoiesis & Translational Research: blood cell biology, multi-omic approaches, and translational studies.
Contact (+33) 1 81 72 43 14 sara.bencheikh@inserm.fr
Location Hôpital Necker – Enfants Malades 149 rue de Sèvres 75015 Paris
Our team investigates the biology of blood group antigens and the pathophysiology of sickle cell disease, with a particular focus on hematopoiesis and inflammatory anemia. By studying how blood cells develop and function under both physiological and pathological conditions, we aim to better understand the mechanisms that drive anemia and chronic inflammation.
Our research seeks to identify key molecules and signaling pathways that contribute to disease progression. We have shown that the genetic and cellular determinants of blood phenotypes provide essential insights into protein function and disease mechanisms, highlighting how variations in blood group antigens can influence biological processes and clinical outcomes.
In addition, we explore how chronic inflammation contributes to both acute and long-term complications of sickle cell disease, including vaso-occlusive crises and splenic dysfunction. Our work also investigates the role of metabolite transporters in regulating blood cell development and in promoting fetal hemoglobin activation, a key therapeutic target for improving disease outcomes.
Our research investigates the regulation of hematopoiesis and erythropoiesis under inflammatory conditions, with a particular focus on sickle cell disease. We examine the impact of inflammation, genetic variation, and metabolic pathways on hematopoietic stem and progenitor cell commitment and erythroid maturation. Special attention is given to early life stages, where hematopoietic dysfunction and impaired maturation can shape disease trajectory in infants with sickle cell disease. By identifying molecular regulators of erythropoiesis and fetal hemoglobin induction, our work aims to uncover new mechanisms that could improve red blood cell production and ameliorate anemia.
Chronic inflammation plays a central role in the pathophysiology of sickle cell disease and its systemic complications. Our work focuses on the cellular and molecular mechanisms that promote vaso-occlusion, endothelial activation, and tissue damage. We investigate how inflammatory cells, cytokine signaling, and red blood cell alterations contribute to vascular obstruction and chronic complications such as leg ulcers. In parallel, we explore how spleen dysfunction emerges at the crossroads of immune dysregulation, abnormal red cell retention, and alloimmunization, providing new insights into the role of the spleen in disease progression.
Our research focuses on the molecular diversity and functional biology of blood group antigens. We investigate the genetic polymorphisms underlying blood group variation and their impact on protein function, red blood cell physiology, and immune recognition. Understanding these mechanisms is particularly important in patients requiring chronic transfusion therapy, such as those with sickle cell disease. By combining genomic approaches with immunohematology, our work aims to improve transfusion compatibility, identify rare blood phenotypes, and enhance transfusion safety for patients at risk of alloimmunization.
This project explores how metabolic pathways regulate erythroid differentiation and fetal hemoglobin induction. By combining functional genomics and multi-omics approaches, we aim to identify key regulators of red blood cell development and potential therapeutic targets for anemia.
We investigate how inflammatory cells, cytokines, and endothelial activation contribute to vaso-occlusive events in sickle cell disease. This project aims to better understand the mechanisms driving vascular obstruction and chronic complications.
This project examines how spleen dysfunction affects immune regulation, red blood cell retention, and alloimmunization in patients with sickle cell disease, providing new insights into disease progression.
