IRF5 and glomerulonephritis: In further support of this, knockout of IRF5 was sufficient to attenuate TLR-induced cytokine production from DCs in vitro (Lyn-/-IRF5-/-), and monoallelic loss of IRF5 was sufficient to abrogate glomerulonephritis in vivo (Lyn-/-IRF5+/-) (73, 118), likely through suppressing transcription of proinflammatory cytokines, IFN-I, and oxidative phosphorylation pathway genes (118).