Background Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency
characterized by eczema, infections, and susceptibility to autoimmunity and malignancies.
Thrombocytopenia is a constant finding, but its pathogenesis remains elusive. Objective To
dissect the basis of the WAS platelet defect, we used a novel conditional mouse model
(CoWas) lacking Wiskott-Aldrich syndrome protein (WASp) only in the megakaryocytic
lineage in the presence of a normal immunologic environment, and in parallel we analyzed …