Pro-inflammatory cytokines (e.g., IL-6 and TNF-α) and chemokines (e.g., CCL2 and CXCL12) activate fibroblasts, leading to excessive collagen deposition and driving fibrosis.[4] Additionally, SLE-associated vasculitis and tissue hypoxia may exacerbate fibrosis through the activation of hypoxia-inducible factor-1α (HIF-1α) and inhibition of local angiogenesis.[16] Autoantibodies in SLE, such as anti-double-stranded DNA antibodies, may cross-react with local antigens. This evidence concerns the gene CCL2 and vasculitis.