New Study Suggests KLF2 May Play a Role in Neutrophil Regulation and the Development of Systemic Lupus Erythematosus

Neutropenia, a condition characterized by low neutrophil levels, is common in individuals with systemic lupus erythematosus (SLE) and can lead to severe infections. A new study investigates the role of Krüppel-like factor 2 (KLF2, a protein coding gene involved in a variety of regulatory pathways and plays a role in controlling inflammation) in regulating neutrophil apoptosis (cell death) and its connection to disease activity in people with SLE. 

The study included 155 participants:  68 with SLE, 57 disease controls (29 with rheumatoid arthritis; 26 with Sjorgen’s Syndrome), and 30 healthy controls. Researchers collected blood samples from each study participant, separated neutrophils, , and analyzed their rates of apoptosis.. They found that people with SLE had blood neutrophil counts that were significantly reduced, which was inversely linked to the SLE disease severity. The findings suggest that KLF2 in neutrophils may be closely related to the development and progression of SLE. The correlation between KLF2 and neutrophil apoptosis suggests that the decline of KLF2 levels may lead to neutropenia in people with SLE. 

This is the first study to show that KLF2 can regulate the apoptosis of neutrophils. Further research is needed to provide insights into the detailed mechanisms leading to the occurrence and development of SLE. Additionally, this study highlights the potential of KLF2 in autoimmunity and as a therapeutic target. Learn more about lupus and inflammation.