Abstract
Autoimmune cytopenias are a consequence of autoantibodies that target blood cell lineages and mark them for their accelerated destruction, mostly through phagocytosis by monocytes and macrophages and complement activation. Neutrophils, although equipped with Fc and complement receptors and effector mechanisms that are critical in other autoimmune conditions, remained long overlooked. Recent reports, however, propose a new and possibly critical role of neutrophils. In this review, we gathered available evidence on the contribution of neutrophils to the development, onset, and consequences of autoantibody-dependent cytopenias.
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