This is in keeping with the study by Manzanillo et al., who reported an increase in IL-1β 3 weeks after infection in the serum of mice that lacked IRF3 (a transcription factor activated downstream following pathogen recognition by RNA sensors), but in contrast with the study by Cheng and Schorey, who found a RIG-I–dependent decrease in IFN-β in alveolar macrophages from mice that lacked the downstream signaling adaptor MAVS 2 weeks after M. tuberculosis infection (16, 20). This evidence concerns the gene IL1B and infection.