Nat. Immunol. 11, 63–69 (2010); published online 15 November 2009; addendum published after print 15 May 2013

In 2010 we reported in Nature Immunology how the sensing of cytosolic RNA triggers the generation of mature interleukin 1β (IL-1β; Poeck et al., Nat. Immunol. 11, 63–69 (2010)). We demonstrated that ligation of the RNA helicase RIG-I triggered the adaptor CARD9 downstream of the signaling adaptor MAVS (IPS-1) to induce the transcription factor NF-κB for the generation of pro-IL-1β and in parallel activated caspase-1 for the generation of mature IL-1β. We presented data that indicated similar generation of pro-IL-1β and IL-1β in wild-type bone marrow–derived dendritic cells (BMDCs) and BMDCs deficient in CARD9 or the adaptor Bcl-10 after transfection of the synthetic DNA poly(dA:dT) (Fig. 3c (right) and Fig. 4c,e,f). However, additional experiments in our laboratory have shown that CARD9- or Bcl-10-deficient BMDCs have impaired production of pro-IL-1β and IL-1β not only after sensing of RNA but also after the transfection of poly(dA:dT). We speculate that a particular aliquot of poly(dA:dT) used during the preparation of our study published in 2010 might have been contaminated with lipopolysaccharide or some other CARD9-independent trigger of the innate immune system. Still, the central conclusions of that manuscript (that RIG-I signals via CARD9 and the inflammasome to control IL-1β) remain unchanged and have been confirmed by multiple independent laboratories. Nevertheless, we would like to correct the idea that CARD9- or Bcl-10-deficient cells have normal IL-1β responses to the transfection of poly(dA:dT).