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The role of neutrophils in skin damage induced by tissue‐deposited lupus IgG

Summary Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Neutrophils are crucial effector cells in the immune system but the significance of neutrophils in the pathogenesis of SLE is not clear. This study is to explore the role of neut...

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Bibliographic Details
Published in:Immunology 2018-08, Vol.154 (4), p.604-612
Main Authors: Guo, Xuanxuan, Fang, Xiang, He, Guodan, Zaman, Muhammad Haidar, Fei, Xibin, Qiao, Wei, Deng, Guo‐Min
Format: Article
Language:English
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Summary:Summary Skin injury is the second most common clinical manifestation in patients with systemic lupus erythematosus (SLE). Neutrophils are crucial effector cells in the immune system but the significance of neutrophils in the pathogenesis of SLE is not clear. This study is to explore the role of neutrophils in the skin damage of SLE. We used lupus‐prone mice and a C57BL/6 mouse model of lupus serum IgG‐induced skin inflammation to investigate the role of neutrophils in skin damage of SLE. We found that a few neutrophils infiltrated the inflammatory sites of skin in lupus‐prone mice and the lupus‐IgG‐induced skin damage mouse model. Depletion of neutrophils did not affect the development of skin inflammation caused by lupus IgG, and lupus IgG can induce apoptosis of neutrophils. The apoptosis of neutrophils induced by lupus IgG is related to FcγRIII and Fas/Fas ligand pathways. Our study indicates that neutrophils are not major contributors in the skin damage caused by tissue‐deposited lupus IgG but death of neutrophils caused by lupus IgG may provide a resource of a large amount of autoantigens in SLE. Neutrophils do not exert a crucial role in the development of skin damage induced by skin‐deposited lupus IgG, but neutrophils may play a key role in production of high levels of autoantibodies in systemic lupus erythematosus by providing autoantigens because lupus IgG can induce apoptosis of neutrophils.
ISSN:0019-2805
1365-2567
DOI:10.1111/imm.12908