A new animal model of systemic sclerosis

为了评估抗DNA拓扑异构酶I（anti-topo I）抗体的贡献，在用topo I和弗氏完全佐剂（CFA）或弗氏不完全佐剂（IFA）处理的小鼠中检查组织纤维化和细胞因子产生。与用topo I和IFA处理相比，用topo I和CFA处理诱导皮肤和肺纤维化，同时增加白细胞介素（IL）-6和IL-17产生。Topo I和CFA处理组小鼠的抗Topo I抗体水平高于Topo I和IFA处理组; Topo I和CFA处理组小鼠支气管肺泡灌洗液中Th 2和Th 17细胞频率增加，而Topo I和IFA处理组小鼠支气管肺泡灌洗液中Th 1和Treg细胞频率增加; IL-6表达缺失可改善皮肤和肺纤维化，并降低Th 2和Th 17细胞频率。这项研究表明，用topo I和CFA治疗诱导Ssc样组织纤维化和自身免疫。

To assess the contribution of anti-DNA topoisomerase I(anti-topo I)antibody, tissue fibrosis and cytokine production were examined in mice treated with topo I and either Freund's complete adjuvant (CFA) or Freund's incomplete adjuvant(IFA).Treatment with topo I and CFA,in contrast to treatment with topo I and IFA,induced skin and lung fibrosis with increased interleukin (IL)-6 and IL-17 production. Anti-topo I antibody levels were greater in mice treated with topo I and CFA than with topo I and IFA.Furthermore,treatment with topo I and CFA increased Th2 and Th17 cell frequencies in bronchoalveolar lavage fluid,whereas treatment with topo I and IFA increased Th1 and Treg cell frequencies.Moreover,loss of IL-6 expression ameliorated skin and lung fibrosis and decreased Th2 and Th17 cell frequencies. This study shows that treatment with topo I and CFA induces SSc-like tissue fibrosis and autoimmunity.