IFNA1 and systemic lupus erythematosus: Constitutive depletion of pDCs in lupus-prone mice either through genetic ablation of IRF8, a transcription factor required for pDC and CD8αDC development, or by diphtheria toxin treatment of mice expressing the diphtheria toxin receptor on pDCs resulted in markedly reduced type I IFN production, a reduced IFN signature, reduced autoantibody production, and reduction in the severity of kidney pathology glomerulonephritis [124–126].