关键词：血管生成；关节炎；将细胞（生物）
摘 要：Production of IL-17 from joint TH-17 cells can strongly contribute to RA angiogenesis (4) through a mechanism that is in part due to induction of VEGF from RA ST fibroblasts (5, 6). We document that CCL21 is expressed from endothelial cells activated by IL-17 (23) and neutralization of CCL21 markedly reduces IL-17 mediated VEGF transcription from the RA ST. Like IL-17, CCL21 is also capable of enhancing production of VEGF from RA ST fibroblasts and can further synergize with VEGF in facilitating endothelial chemotaxis. Hence CCL21 may be the unidentified connecting factor between the IL-17 and VEGF cascades. Therapeutic targeting of VEGF and VEGFR has led to disappointing results regarding drug toxicity and lack of efficacy in patients with advanced tumor growth (24, 25) therefore RA patients were not treated with anti-VEGF or anti- VEGFR therapies. However, since we demonstrate that CCL21 induced by IL-17 can modulate VEGF expression in RA ST, targeting CCL21 may disconnect the link between IL-17 and VEGF cascade and therefore more efficiently suppress RA neovascularization.