机构:[1]Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, China,[2]Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, United States,[3]Center for Cutaneous Biology and Immunology Research, Department of Dermatology, Henry Ford Health System, Detroit, MI, United States,[4]Department of Rheumatology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China,[5]Department of Gerontology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China,[6]Department of Internal Medicine, Henry Ford Health System, Detroit, MI, United States
Gout is an inflammatory arthritis caused by deposition of intra-articular monosodium urate (MSU) crystal. Previous studies have focused on resident macrophage, infiltrating monocyte, and neutrophil responses to MSU crystal; yet the mechanisms of cellular changes and the potential involvement of other regulatory immune cells remain largely unknown. Invariant natural killer T (iNKT) cells, an innate type of T cell, are involved in the development of various inflammatory diseases. Here, we investigate the role of iNKT cells in MSU crystal-induced gouty inflammation. MSU crystal-induced inflammatory profiles in an air-pouch model were examined in iNKT-deficient CD1d knockout (KO) and wild-type (WT) control mice. To explore potential mechanisms of iNKT cell regulation of gouty inflammation, we cocultured CD4+ or CD4-iNKT cells with bone marrow-derived macrophages (BMDMs). We found that iNKT cells quickly migrated to the site of inflammation upon MSU crystal stimulation in WT mice. The total number of infiltrating cells in CD1d KO mice, especially neutrophils, was dramatically increased at 6 and 12 h (P < 0.01) post-MSU crystal challenge, compared with WT controls. BMDMs cocultured with CD4+iNKT cells produced less tumor necrosis factor-α and expressed higher levels of M2 macrophage markers, including Clec7a, Pdcd1Ig2, and interleukin-4 (P < 0.01), compared with BMDMs cocultured with CD4-iNKT cells or conventional CD4+ T cells. CD4+iNKT cells are one of the key regulators of MSU crystal-induced gouty inflammation through the control of macrophage polarization. iNKT cells may serve as a new therapeutic target for gout.
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外文
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出版当年[2017]版:
大类|2 区医学
小类|2 区免疫学
最新[2023]版:
大类|2 区医学
小类|2 区免疫学
第一作者:
第一作者机构:[1]Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, China,[2]Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, United States,[3]Center for Cutaneous Biology and Immunology Research, Department of Dermatology, Henry Ford Health System, Detroit, MI, United States,
共同第一作者:
通讯作者:
通讯机构:[1]Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, China,[2]Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, United States,[3]Center for Cutaneous Biology and Immunology Research, Department of Dermatology, Henry Ford Health System, Detroit, MI, United States,[4]Department of Rheumatology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China,[6]Department of Internal Medicine, Henry Ford Health System, Detroit, MI, United States
推荐引用方式(GB/T 7714):
Wang Jie,Yang Qibin,Zhang Quanbo,et al.Invariant Natural Killer T Cells Ameliorate Monosodium Urate Crystal-Induced Gouty Inflammation in Mice.[J].Frontiers in immunology.2017,8:1710.doi:10.3389/fimmu.2017.01710.
APA:
Wang Jie,Yang Qibin,Zhang Quanbo,Yin Congcong,Zhou Li...&Mi Qing-Sheng.(2017).Invariant Natural Killer T Cells Ameliorate Monosodium Urate Crystal-Induced Gouty Inflammation in Mice..Frontiers in immunology,8,
MLA:
Wang Jie,et al."Invariant Natural Killer T Cells Ameliorate Monosodium Urate Crystal-Induced Gouty Inflammation in Mice.".Frontiers in immunology 8.(2017):1710