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Similar to the abnormal basal keratinocytes of patients, DCs in the skin lesions of model mice are overactivated by type I IFNs derived from keratinocytes, and this overactivation is sufficient to drive the onset of SLE [103]
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Next, inhibition of HIF1a expression by siRNA in cultured THP-1 and Raw cell macrophages led to upregulation of STAT6 target genes, suggesting a switch to an anti-inflammatory polarization
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