DC hyperactivation might also result from environmental triggers such as an inflammatory cytokine milieu induced by bacteria (86, 87), excessive IFN production in response to viral infection as observed in DM1 (88), oxidative stress induced by noxious agents as observed in RA (89) or danger signals released under cell stress or from necrotic and late apoptotic cells as documented in SLE and DM1 (90, 91). Here, IFNA1 is linked to systemic lupus erythematosus.