IgG sialylation puts lung inflammation to REST

The mechanisms underpinning susceptibility to influenza virus infection, resulting in life-threatening disease, are not well understood. In this issue of Immunity, Chakraborty et al. demonstrate that sialylated IgG suppresses NF-κB-driven inflammatory responses in the lungs by inducing repressor element-1 silencing transcription factor (REST) to prevent excessive inflammation without impacting viral replication. The mechanisms underpinning susceptibility to influenza virus infection, resulting in life-threatening disease, are not well understood. In this issue of Immunity, Chakraborty et al. demonstrate that sialylated IgG suppresses NF-κB-driven inflammatory responses in the lungs by inducing repressor element-1 silencing transcription factor (REST) to prevent excessive inflammation without impacting viral replication.