Wiskott-Aldrich Syndrome (WAS) is an X-linked primary immunodeficiency caused by mutations in the WAS gene, leading to impaired expression or function of the WAS protein (WASp) and consequent cytoskeletal dysregulation in hematopoietic cells. This results in defective cellular responses, including impaired cell signalling, migration, and activation. To further investigate how hypomorphic WAS mutations impact immune cell development and function, we established an induced pluripotent stem cell (iPSC)-based model system. iPSCs bearing defined WAS mutations identified in patients were generated and differentiated into various hematopoietic lineages in vitro and characterized using phenotypic, transcriptomic, and functional assays. Our differentiation platform recapitulated key functional deficits observed in patient-derived macrophages, T cells, and natural killer (NK) cells, and revealed previously unreported abnormalities in cell differentiation, proliferation and activation. Notably, we observed an increased differentiation kinetics in neutrophil and megakaryocyte lineages from WASp-deficient cells. This work provides new insights into the mechanistic basis of immune dysregulation in WAS, and has established a robust platform for tracking immune cell development in vitro and for preclinical evaluation of potential gene therapies.