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首页> 美国卫生研究院文献>Wiley-Blackwell Online Open >Interleukin‐6 receptor alpha blockade improves skin lesions in a murine model of systemic lupus erythematosus
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Interleukin‐6 receptor alpha blockade improves skin lesions in a murine model of systemic lupus erythematosus

机译：白细胞介素-6受体α阻滞改善系统性红斑狼疮小鼠模型的皮肤损伤

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Systemic lupus erythematosus (SLE) is an autoimmune disease, characterized by antinuclear autoantibodies (ANA) and immunocomplexes, commonly affecting kidneys, skin, heart, lung or even the brain. We have shown that JunBΔep mice develop a SLE phenotype linked to increased epidermal Interleukin (IL)‐6 secretion. Blocking of IL‐6 receptor alpha (IL‐6Rα) is considered as therapeutic strategy for the treatment of SLE. JunBΔep and wild‐type mice were treated for short (5 weeks) or long term (21 weeks) with the IL‐6Rα‐blocking antibody MR16‐1. Skin and kidney of mice were investigated by histology and immunofluorescence, and in addition, kidneys were analysed by electron microscopy. Furthermore, soluble IL‐6R (sIL‐6R), antihistone and antinucleosome antibodies levels were measured and associated with disease parameters. Treatment with MR16‐1 resulted in significant improvement of SLE‐like skin lesions in JunBΔep mice, compared to untreated mice. The sIL‐6R amount upon long‐term treatment with MR16‐1 was significantly higher in JunBΔep versus untreated JunBΔep (P = 0.034) or wild‐type mice (P = 0.034). MR16‐1 treatment over these time spans did not significantly improve kidney pathology of immunoglobulin deposits causing impaired function. Significantly higher antihistone (P = 0.028) and antinucleosome antibody levels (P = 0.028) were measured in style="fixed-case">MR16‐1‐treated JunBΔep mice after treatment compared to levels before therapy. In conclusion, blockade of style="fixed-case">IL‐6Rα improves skin lesions in a murine style="fixed-case">SLE model, but does not have a beneficial effect on autoimmune‐mediated kidney pathology. Inhibition of style="fixed-case">IL‐6R signalling might be helpful in lupus cases with predominant skin involvement, but combinatorial treatment might be required to restrain autoantibodies.
机译：系统性红斑狼疮（SLE）是一种自身免疫性疾病，其特征在于抗核自身抗体（ANA）和免疫复合物，通常会影响肾脏，皮肤，心脏，肺部甚至大脑。我们已经证明，JunB Δep小鼠发展出与表皮白介素（IL）-6分泌增加有关的SLE表型。阻断IL-6受体α（IL-6Rα）被视为治疗SLE的治疗策略。使用IL-6Rα阻断抗体MR16-1对JunB Δep和野生型小鼠进行了短期（5周）或长期（21周）治疗。通过组织学和免疫荧光检查小鼠的皮肤和肾脏，此外，通过电子显微镜检查肾脏。此外，还测量了可溶性IL-6R（sIL-6R），抗组蛋白和抗核小体抗体的水平，并与疾病参数相关。与未经治疗的小鼠相比，使用MR16-1进行治疗的JunB Δep小鼠可显着改善SLE样皮肤病变。长期用MR16-1治疗的sIL-6R量在JunB Δep中显着高于未治疗的JunB Δep（P = 0.034）或野生型小鼠（P = 0.034）。在这些时间段内，MR16-1治疗并未显着改善免疫球蛋白沉积物导致功能受损的肾脏病理。在 style =“ fixed-case”> MR 16-1治疗的JunB Δep小鼠中，测得的抗组蛋白（P = 0.028）和抗核小体抗体水平（P = 0.028）明显更高治疗后与治疗前的水平相比。总之，在小鼠 style =“ fixed-case”> SLE 模型中，对 style =“ fixed-case”> IL -6Rα的阻滞可改善皮肤病变，但没有对自身免疫介导的肾脏病理的有益作用。抑制 style =“ fixed-case”> IL -6R信号可能在皮肤受累占主要的狼疮病例中有所帮助，但可能需要联合治疗以抑制自身抗体。

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