TLR3 and infection: Since OTUB1-competent BMDCs showed stronger activation of TAK1 and production of the cytokines IL-12, TNF, and IL-6 upon engagement of TLR2, TLR7, TLR9, and IL-1R, all of which signal via MyD88, and upon TNF stimulation and poly I:C-induced TLR3 activation, both of which induce MyD88-independent signaling, OTUB1 may contribute to proinflammatory DC responses in a wide range of infections and inflammatory disorders.