The role of IL-1 in skin inflammation induced by lupus serum
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- 英文论文题名：The role of IL-1 in skin inflammation induced by lupus serum
- 论文作者：Li Xiaoyan ; Guo Xuanxuan ; Liu Huicheng ; Xu Guangqiong ; Fei Xibing ; Deng Guo-Min
- 英文论文作者：Li Xiaoyan ; Guo Xuanxuan ; Liu Huicheng ; Xu Guangqiong ; Fei Xibing ; Deng Guo-Min ; Nanjing Medical University
- 年：2016
- 作者机构：Nanjing Medical University;
- 英文论文关键词：Systemic lupus erythematosus ; Skin inflammation ; IL-1 ; lupus serum
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R593.241
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1302k
- 原文格式：D
- 会议级别：全国
摘要
Objectives: Systemic lupus erythematosus(SLE) is a seriously chronic autoimmune disease, which is characterized by a large number of autoantibodies and multiple organ damage. Skin lesion is one of the common clinical manifestations of lupus erythematosus, but its pathogenesis is not clear. IL-1 is a proinflammatory cytokine, and its role in SLE skin lesion is still unclear.Methods: We used IL-1 receptor deficient mice and other gene deficient mice to study the role of IL-1 in the lupus serum-induced skin inflammation. Results: We found that the severity of skin lesion in IL-1 receptor deficient mice and caspase-1 deficient mice was reduced compared with that in wild type mice. IL-1 receptor deficiency suppressed the expression of FcγRI(CD64) and MHC class II(CD74), and increased the level of FcγRII(CD32) induced by lupus serum. IL-1 receptor deficiency also suppressed the lipid raft clustering and IFN-γ in T cells, and reduced IgG internalization and presentation in macrophage, and decreased expression of MCP-1 and TNFa in monocytes. In addition, TNFa couldpromote the proliferation of kerationocytes.Conclusions: Our findings indicate that IL-1 plays an important role in skin lesions of lupus erythematosus. This study suggests IL-1 is a therapeutic target in skin lesions of systemic lupus erythematosus.
Objectives: Systemic lupus erythematosus(SLE) is a seriously chronic autoimmune disease, which is characterized by a large number of autoantibodies and multiple organ damage. Skin lesion is one of the common clinical manifestations of lupus erythematosus, but its pathogenesis is not clear. IL-1 is a proinflammatory cytokine, and its role in SLE skin lesion is still unclear.Methods: We used IL-1 receptor deficient mice and other gene deficient mice to study the role of IL-1 in the lupus serum-induced skin inflammation. Results: We found that the severity of skin lesion in IL-1 receptor deficient mice and caspase-1 deficient mice was reduced compared with that in wild type mice. IL-1 receptor deficiency suppressed the expression of FcγRI(CD64) and MHC class II(CD74), and increased the level of FcγRII(CD32) induced by lupus serum. IL-1 receptor deficiency also suppressed the lipid raft clustering and IFN-γ in T cells, and reduced IgG internalization and presentation in macrophage, and decreased expression of MCP-1 and TNFa in monocytes. In addition, TNFa couldpromote the proliferation of kerationocytes.Conclusions: Our findings indicate that IL-1 plays an important role in skin lesions of lupus erythematosus. This study suggests IL-1 is a therapeutic target in skin lesions of systemic lupus erythematosus.
Objectives: Systemic lupus erythematosus(SLE) is a seriously chronic autoimmune disease, which is characterized by a large number of autoantibodies and multiple organ damage. Skin lesion is one of the common clinical manifestations of lupus erythematosus, but its pathogenesis is not clear. IL-1 is a proinflammatory cytokine, and its role in SLE skin lesion is still unclear.Methods: We used IL-1 receptor deficient mice and other gene deficient mice to study the role of IL-1 in the lupus serum-induced skin inflammation. Results: We found that the severity of skin lesion in IL-1 receptor deficient mice and caspase-1 deficient mice was reduced compared with that in wild type mice. IL-1 receptor deficiency suppressed the expression of FcγRI(CD64) and MHC class II(CD74), and increased the level of FcγRII(CD32) induced by lupus serum. IL-1 receptor deficiency also suppressed the lipid raft clustering and IFN-γ in T cells, and reduced IgG internalization and presentation in macrophage, and decreased expression of MCP-1 and TNFa in monocytes. In addition, TNFa couldpromote the proliferation of kerationocytes.Conclusions: Our findings indicate that IL-1 plays an important role in skin lesions of lupus erythematosus. This study suggests IL-1 is a therapeutic target in skin lesions of systemic lupus erythematosus.
引文