Project

Immune thrombocytopenia (ITP) is an autoimmune disease characterized by autoantibodies targeting platelets resulting in a low platelet count and an increased risk of bleeding. Platelet phagocytosis is mediated by antibody platelet opsonization and complement activation. Although neutrophils are professional phagocytes and are functionally equipped to act at different steps of ITP, their contribution to the disease remains understudied. Neutrophils express complement and Fc receptors and can phagocytose platelets. Moreover, neutrophils accumulate in the spleen of ITP patients where they settle in proximity to a specific B cell subset. Previous studies have suggested a role for neutrophils in the regulation of adaptive immunity especially in B cell activation and proliferation: In the spleen, “B helper neutrophils” can produce cytokines such as interleukin-21 (IL-21), B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) that induce B cell maturation into antibody-secreting plasma cells. These elements strongly support the implication of neutrophils in ITP. The objective of our project is to identify differentially expressed genes in neutrophils from ITP patients versus healthy donors to better understand their implication in the pathophysiology of ITP.