Skin inflammation induced by lupus serum was inhibited in IL-1R deficient mice

被引：9
作者：
Li, Xiaoyan [1 ]
Guo, Xuanxuan [1 ]
Liu, Huicheng [1 ]
Gao, Gongming [1 ]
Xu, Guangqiong [1 ]
Fei, Xibin [1 ]
Fang, Xiang [1 ]
Qiao, Wei [1 ]
Deng, Guo-Min [1 ,2 ]
机构：
[1] Nanjing Med Univ, Key Lab Antibody Tech, Minist Hlth, Nanjing 211166, Jiangsu, Peoples R China
[2] Nanjing Med Univ, State Key Lab Reprod Med, Nanjing, Jiangsu, Peoples R China
来源：
CLINICAL IMMUNOLOGY | 2017年 / 180卷
关键词：
Systemic lupus erythematosus (SLE); IL-1 receptor deficient mice; Lupus serum; Skin inflammation; INTERLEUKIN-1 RECEPTOR ANTAGONIST; LIPID RAFTS; CELL ACTIVATION; AUTOIMMUNE MICE; MRL/LPR MICE; PRONE MICE; T-CELLS; ERYTHEMATOSUS; DISEASE; PATHOGENESIS;
D O I：
10.1016/j.clim.2017.03.015
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Skin inflammation induced by lupus serum is a useful tool to investigate the pathogenesis of lupus skin injury. IL-1 is a proinflammatory cytoldne, 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 Fc gamma RI (CD64), Fc gamma RII (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 TNF alpha. in monocytes. Keratinocyte proliferation induced by lupus serum was significantly decreased in TNF alpha 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. (C) 2017 Elsevier Inc. Affrights reserved.
引用
收藏
页码：63 / 68
页数：6
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