Editorials and Perspectives

Myelodysplastic syndromes (MDS), first clearlydefined as an entity by the pioneering studiesof Bernard Dreyfus and others, have long been perceived as pre-leukemic hematopoietic stem cell abnormalities which cause bone marrow failure and ulti-mately transform to acute leukemia. The bone marrow failure, resulting in the transfusion dependence and neutropenic infection that characterizes the disease, was assumed to be an intrinsic stem cell defect causing defective maturation. However, accumu-lating evidence has shown that marrow failure in some MDS is associated with autoimmunity, T-cell mediated myelosuppression and cytokine-induced cytopenias. The novel study by Chamuleau et al.1 in this issue sug-gests that the innate immune system may play a role in MDS pathophysiology. Study of the autoimmune com-ponent in MDS pathophysiology has led to better defi