STAT3 mutations and persistence of autoimmunity

Abstract

In this issue of Blood, Jerez et al show that signal transducer and activator of transcription 3 (STAT3) mutations resulting in persistent proliferation of cytotoxic autoimmune T-cell clones as seen in large granular lymphocytic (LGL) leukemia is present in the autoimmune disorders acquired aplastic anemia (AA) and myelodysplastic syndrome (MDS).1 © 2013 by The American Society of Hematology.