Analogously, C4BP(β-)- and PRP6-HO7-treated Mo-DCs isolated from active LN patients and matured with LPS or gardiquimod downregulated not only surface activation markers (CD83, CD86, CD80, CD40), but also pro-inflammatory cytokines such as TNF-α and IL-12 (the latter only through LPSactivation, although it did not reach statistical significance) (Figure 8). This evidence concerns the gene CD86 and lobular neoplasia.