The lazy leukocyte syndrome revisited

Abstract

In this issue of Blood, Kuhns et al1 describe the probable molecular and genetic basis for a disease that has mystified investigators for over 45 years, the lazy leukocyte syndrome. This disorder is characterized by recurrent infections, stomatitis, a low neutrophil count, and impaired neutrophil motility,2-5 and these abnormalities can now be explained by mutations in actin-interacting protein 1 (Aip1).1 This natural experiment provides exciting new insights into how neutrophils and other nonmuscle cells regulate their actin filament architecture to change shape and migrate.