狼疮血清引起的皮肤炎症在白细胞介素-1 受体缺陷小鼠中受到抑制。
Skin inflammation induced by lupus serum was inhibited in IL-1R deficient mice.
机构信息
Key Laboratory of Antibody Techniques of Ministry of Health, Nanjing Medical University, Nanjing, China.
Key Laboratory of Antibody Techniques of Ministry of Health, Nanjing Medical University, Nanjing, China; State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
出版信息
Clin Immunol. 2017 Jul;180:63-68. doi: 10.1016/j.clim.2017.03.015. Epub 2017 Apr 7.
Skin inflammation induced by lupus serum is a useful tool to investigate the pathogenesis of lupus skin injury. IL-1 is a proinflammatory cytokine, and its role in lupus skin lesion is still unclear. We determined the role of IL-1 in lupus skin injury by using gene deficient mice. We found that skin inflammation induced by lupus serum was significantly reduced in IL-1R deficient mice and caspase-1 deficient mice. IL-1R deficiency did not affect the expression of FcγRI (CD64), FcγRII (CD32) and MHC class II (CD74) induced by lupus serum. IL-1R deficiency reduced the lipid raft clustering, and decreased expression of MCP-1 and TNFα in monocytes. Keratinocyte proliferation induced by lupus serum was significantly decreased in TNFα deficient mice. Our findings indicate that IL-1 plays an important role in skin lesions of SLE. This study suggests that IL-1 is a therapeutic target in skin lesions of SLE.
狼疮血清引起的皮肤炎症是研究狼疮皮肤损伤发病机制的有用工具。IL-1 是一种促炎细胞因子，但其在狼疮皮肤病变中的作用尚不清楚。我们通过基因缺陷小鼠来确定 IL-1 在狼疮皮肤损伤中的作用。我们发现，狼疮血清诱导的皮肤炎症在 IL-1R 缺陷小鼠和 caspase-1 缺陷小鼠中显著减轻。IL-1R 缺陷不影响狼疮血清诱导的 FcγRI（CD64）、FcγRII（CD32）和 MHC Ⅱ类（CD74）的表达。IL-1R 缺陷减少了单核细胞中脂质筏的聚集，并降低了 MCP-1 和 TNFα 的表达。狼疮血清诱导的角质形成细胞增殖在 TNFα 缺陷小鼠中显著降低。我们的研究结果表明，IL-1 在 SLE 的皮肤病变中发挥重要作用。这项研究表明，IL-1 是 SLE 皮肤病变的治疗靶点。
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