邮件订阅 RSS

留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

巨噬细胞参与系统性硬化症发病机制的研究进展

苏敏慧,  郭峰,  钱先

downloadPDF
文章导航 > 协和医学杂志  > 2019 >  10(3): 278-283
苏敏慧, 郭峰, 钱先. 巨噬细胞参与系统性硬化症发病机制的研究进展[J]. 协和医学杂志, 2019, 10(3): 278-283. doi: 10.3969/j.issn.1674-9081.2019.03.016
引用本文: 苏敏慧, 郭峰, 钱先. 巨噬细胞参与系统性硬化症发病机制的研究进展[J]. 协和医学杂志, 2019, 10(3): 278-283. doi: 10.3969/j.issn.1674-9081.2019.03.016
shu
Min-hui SU, Feng GUO, Xian QIAN. Macrophage Involvement and Its Pathogenesis in Systemic Sclerosis[J]. Medical Journal of Peking Union Medical College Hospital, 2019, 10(3): 278-283. doi: 10.3969/j.issn.1674-9081.2019.03.016
Citation: Min-hui SU, Feng GUO, Xian QIAN. Macrophage Involvement and Its Pathogenesis in Systemic Sclerosis[J]. Medical Journal of Peking Union Medical College Hospital, 2019, 10(3): 278-283. doi: 10.3969/j.issn.1674-9081.2019.03.016
shu

巨噬细胞参与系统性硬化症发病机制的研究进展

doi: 10.3969/j.issn.1674-9081.2019.03.016
  • 1.

    南京中医药大学第一临床医学院, 南京 210023

  • 2.

    南京中医药大学附属医院江苏省中医院风湿科, 南京 210029

基金项目: 

江苏省中医院院内项目 Y17035

详细信息
    通讯作者:

    钱先 电话:13851444984, E-mail:moneyfirst1@163.com

  • 中图分类号: R593

Macrophage Involvement and Its Pathogenesis in Systemic Sclerosis

  • 1.

    First Clinical College of Nanjing University of Chinese Medicine, Nanjing 210023, China

  • 2.

    Department of Rheumatology, Jiangsu Province Hospital of Chinese Medicine Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China

More Information

    摘要
  • 摘要: 纤维化是系统性硬化症的主要病理改变, 具体机制尚不明确。巨噬细胞在体内通过多种途径参与系统性硬化症的发生发展, 其作用不可忽视。近年来巨噬细胞与该疾病的研究报道多集中于巨噬细胞极化、活化等调节作用及其相关标志物方面, 另外还涉及巨噬细胞与其他免疫细胞、Toll样受体的关系等。本文就上述几方面, 总结了巨噬细胞在系统性硬化症发病机制中的研究进展。
    Abstract: Fibrosis is the characteristic hallmark of systemic sclerosis (SSc). Although the specific mechanism has been unknown, the role of macrophages in the development of this complex disease through various ways cannot be negligible. Findings during the past 5 years have contributed to more understanding of the relationship between macrophages and SSc. This review is mainly about the progress of research on macrophages in SSc. We discuss whether or not macrophages skew toward the M1-like phenotype from the profibrotic M2-like phenotype. Some biomarkers are also listed. In addition, we elaborate on the association of macrophages with other immune cells and Tall-like receptors.
    利益冲突  无
    • HTML全文
    • 参考文献(48)
  • [1] Wu M, Schneider DJ, Mayes MD, et al. Osteopontin in systemic sclerosis and its role in dermal fibrosis[J].J Invest Dermatol, 2012, 132:1605-1614. doi:  10.1038/jid.2012.32
    [2] 黄雁超, 李流云, 崔向清, 等.巨噬细胞在肺纤维化的发病机制研究进展[J].重庆医学, 2015, 44:2999-3002. doi:  10.3969/j.issn.1671-8348.2015.21.044
    [3] O'Reilly S. Toll Like Receptors in systemic sclerosis:An emerging target[J].Immunol lett, 2018, 195:2-8. https://pubmed.ncbi.nlm.nih.gov/28888416/
    [4] Dowson C, Simpson N, Duffy L, et al. Innate Immunity in Systemic Sclerosis[J]. Curr Rheumatol Rep, 2017, 19:2. doi:  10.1007/s11926-017-0630-3
    [5] Ochoa E, Martin JE, Assasi S, et al.Confirmation of CCR6 as a risk factor for anti-topoisomerase Iantibodies in systemic sclerosis[J].Clin Exp Rheumatol, 2015, 33:S31-S35. http://europepmc.org/article/MED/26314374
    [6] O'Reilly S, Cant R, Ciechomska M, et al. Serum amyloid A induces interleukin-6 indermal fibroblasts via Toll-like receptor 2, interleukin-1 receptor-associated kinase 4 and nuclear factor-κB[J].Immunology, 2014, 143:331-340. doi:  10.1111/imm.12260
    [7] Taniguchi T, Asano Y, Akamata K, et al. Fibrosis, vascular activation, and immune abnormalities resembling systemic sclerosis in bleomycin-treated Fli-1-haploinsufficient mice[J]. Arthritis Rheumatol, 2015, 67:517-526. doi:  10.1002/art.38948
    [8] Stenstrom M, Nyhlen HC, Torngren M, et al. Paquinimod reduces skin fibrosis in tight skin 1 mice, an experimental model of systemic sclerosis[J].J Dermatol Sci, 2016, 83:52-59. doi:  10.1016/j.jdermsci.2016.04.006
    [9] Morin F, Kavian N, Chouzenoux S, et al. Leflunomide prevents ROS-induced systemic fibrosis in mice[J]. Free Radic Biol Med, 2017, 108:192-203. doi:  10.1016/j.freeradbiomed.2017.03.035
    [10] Toyama T, Asano Y, Akamata K, et al. Tamibarotene Ameliorates Bleomycin-Induced Dermal Fibrosis by Modulat-ing Phenotypes of Fibroblasts, Endothelial Cells, and Immune Cells[J]. J Invest Dermatol, 2016, 136:387-398. doi:  10.1016/j.jid.2015.10.058
    [11] Maier C, Ramming A, Bergmann C, et al. Inhibition of phosphodiesterase 4(PDE4) reduces dermal fibrosis by interfering with the release of interleukin-6 from M2 macrophages[J].Ann Rheum Dis, 2017, 76:1133-1141. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=a31297be9df3026114fb02726d1fd55e
    [12] Arai M, Ikawa Y, Chujo S, et al. Chemokine receptors CCR2 and CX3CR1 regulate skin fibrosis in the mouse model of cytokine-induced systemic sclerosis[J].J Dermatol Sci, 2013, 69:250-258. doi:  10.1016/j.jdermsci.2012.10.010
    [13] van Bon L, Cossu M, Scharstuhl A, et al. Low heme oxygenase-1 levels in patients withsystemic sclerosis are associated with an altered Toll-like receptor response:another role for CXCL4[J].Rheumatology, 2016, 55:2066-2073. doi:  10.1093/rheumatology/kew251
    [14] Ciechomska M, O'Reilly S, Przyborski S, et al. Histone demethylation and toll-like receptor 8-dependent cross-talk in monocytes promotes transdifferentiation of fibroblasts in systemic sclerosis via Fra-2[J].Arthritis Rheumatol, 2016, 68:1493-1504. doi:  10.1002/art.39602
    [15] O'Reilly S. Epigenetics in fibrosis[J]. Mol Aspects Med, 2017, 54:89-102. doi:  10.1016/j.mam.2016.10.001
    [16] Stifano G, Christmann RB. Macrophage Involvement in Systemic Sclerosis:Do We Need More Evidence?[J]. Curr Rheumatol Rep, 2016, 18:2. doi:  10.1007/s11926-015-0554-8
    [17] Bandinelli F, Del Rosso A, Gabrielli A, et al. CCL2, CCL3 and CCL5 chemokines in systemicsclerosis:the correlation with SSc clinical features and the effect ofprostaglandin E1 treatment[J].Clin Exp Rheumatol, 2012, 30:S44-S49.
    [18] Greenblatt MB, Sargent JL, Farina G, et al. Interspecies comparison of human and murinescleroderma reveals IL-13 and CCL2 as disease subset-specifictargets[J].Am J Pathol, 2012, 180:1080-1094. doi:  10.1016/j.ajpath.2011.11.024
    [19] Assassi S, Wu M, Tan FK, et al.Skin gene expression correlates of severity of interstitial lung disease in systemic sclerosis[J].Arthritis Rheum, 2013, 65:2917-2927. doi:  10.1002/art.38101
    [20] Cai M, Bonella F, He X, et al. CCL18 in serum, BAL fluid and alveolar macrophage culture supernatant in interstitial lung diseases[J]. Respir Med, 2013, 107:1444-1452. doi:  10.1016/j.rmed.2013.06.004
    [21] Mathes AL, Christmann RB, Stifano G, et al.Global chemokine expression insystemic sclerosis (SSc):CCL19 expression correlates with vascular inflammation in SSc skin[J].Ann Rheum Dis, 2014, 73:1864-1872. doi:  10.1136/annrheumdis-2012-202814
    [22] Pickens SR, Chamberlain ND, Volin MV, et al. Characterization of CCL19and CCL21 in rheumatoid arthritis[J].Arthritis Rheum, 2011, 63:914-922. doi:  10.1002/art.30232
    [23] Schneider DJ, Wu M, Le TT, et al. Cadherin-11 contributes to pulmonaryfibrosis:potential role in TGF-beta production and epithelial to mesenchymaltransition[J].FASEB J, 2011, 26:503-512. doi:  10.1096/fj.11-186098
    [24] Wu M, Pedroza M, Lafyatis R, et al. Identification of cadherin 11 as a mediator of dermal fibrosis and possible role in systemic sclerosis[J].Arthritis Rheum, 2014, 66:1010-1021. doi:  10.1002/art.38275
    [25] Corallo C, Paulesu L, Cutolo M, et al. Serum levels, tissue expression and cellular secretion of macrophage migration inhibitory factor in limited and diffuse systemic sclerosis[J]. Clin Exp Rheumatol, 2015, 33:S98-S105. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=d891006e2be83967fc152a84f6440a84
    [26] Wynn TA, Barron L, Thompson RW, et al. Quantitative assessment of macrophage functions in repair and fibrosis[J]. Curr Protoc Immunol, 2011, 14:22.
    [27] Jiao Y, Chen H, Gu T, et al. Molecular network of important genes for systemic sclerosis-related progressive lung fibrosis[J]. BMC Res Notes, 2015, 8:544. doi:  10.1186/s13104-015-1510-4
    [28] Chia JJ, Lu TT. Update on macrophages and innate immunity in scleroderma[J]. Curr Opin Rheumatol, 2015, 27:530-536. doi:  10.1097/BOR.0000000000000218
    [29] Affandi AJ, Radstake TR, Marut W. Update on biomarkers in systemic sclerosis:tools for diagnosis and treatment[J]. Semin Immunopathol, 2015, 37:475-487. doi:  10.1007/s00281-015-0506-4
    [30] Wynn TA, Vannella KM. Macrophages in Tissue Repair, Regeneration, and Fibrosis[J].Immunity, 2016, 4:450-462. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=032056bf12cb83425b03df2bd614c7a1
    [31] Bielecki M, Kowal K, Lapinska A, et al. Increased release of soluble CD163 by the peripheral blood mononuclear cells is associated with worse prognosis in patients with systemic sclerosis[J]. Adv Med Sci, 2013, 58:126-133. doi:  10.2478/v10039-012-0076-9
    [32] Nakayama W, Jinnin M, Makino K, et al. Serum levels of soluble CD163 in patients with systemic sclerosis[J]. Rheumatol Int, 2012, 32:403-407. doi:  10.1007/s00296-010-1691-z
    [33] Bhattacharyya S, Varga J. Emerging roles of innate immune signaling and toll-like receptors in fibrosis and systemic sclerosis[J].Curr Rheumatol Rep, 2015, 17:474. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=7a1519e7a38694c90729fa649b8f025e
    [34] Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity:update on Toll-like receptors[J].Nat Immunol, 2010, 11:373-384. doi:  10.1038/ni.1863
    [35] Heil F, Hemmi H, Hochrein H, et al. Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7and 8[J].Science, 2004, 303:1526-1529. doi:  10.1126/science.1093620
    [36] van Bon L, Affandi AJ, Broen J, et al. Proteome-wide analysis andCXCL4 as abiomarker in systemic sclerosis[J].N Engl J Med, 2014, 370:433-443. doi:  10.1056/NEJMoa1114576
    [37] Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity:update on Toll-like receptors[J].Nat Immunol, 2010, 11:373-384. doi:  10.1038/ni.1863
    [38] Mathes AL, Rice L, Affandi AJ, et al. CpGB DNA activates dermal macrophages and specifically recruits inflammatory monocytes into the skin[J].Exp Dermatol, 2015, 24:133-139. doi:  10.1111/exd.12603
    [39] Stifano G, Affandi AJ, Mathes AL, et al. Chronic Toll-like receptor 4 stimulation in skin induces inflammation, macrophage activation, transforminggrowth factor beta signature gene expression, and fibrosis[J].Arthritis Res Ther, 2014, 16:R136. doi:  10.1186/ar4598
    [40] Bhattacharyya S, Tamaki Z, Wang W, et al. Fibronectin EDA promoteschronic cutaneous fibrosis through Toll-like receptor signaling[J].Sci Transl Med, 2014, 6:232ra50. doi:  10.1126/scitranslmed.3008264
    [41] Takahashi, Asano Y, Ichimura Y, et al. Amelioration of tissue fibrosis by toll-like receptor 4 knockout in murine models of systemic sclerosis[J].Arthritis Rheumatol, 2015, 67:254-265. doi:  10.1002/art.38901
    [42] Kato A, Yutani M, Terao M, et al. Oligosaccharide modification by N-acetylglucosaminyltransferase-V in macrophages are involved in pathogenesis of bleomycin-induced sclerode-rma[J].Exp Dermatol, 2015, 24:585-590. doi:  10.1111/exd.12730
    [43] Morales-Cardenas A, Perez-Madrid C, Arias L, et al. Pulmonary involvement in systemic sclerosis[J]. Autoimmun Rev, 2016, 15:1094-1108. doi:  10.1016/j.autrev.2016.07.025
    [44] Fullard N, O'Reilly S. Role of innate immune system in systemic sclerosis[J].Semin Immunopathol, 2015, 37:511-517. doi:  10.1007/s00281-015-0503-7
    [45] Johnson ME, Pioli PA, Whitfield ML. Gene expression profiling offers insights into the role of innate immune signaling in SSc[J].Semin Immunopathol, 2015, 37:501-509. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=f7ab331bff37ff3783ad23076eed0480
    [46] Christmann RB, Sampaio-Barros P, Stifano G, et al. Association of Interferon- and transforming growth factor beta-regulated genes and macrophage activation with systemic sclerosis-related progressive lung fibrosis[J].Arthritis Rheumatol, 2014, 66:714-725. doi:  10.1002/art.38288
    [47] Juniantito V, Izawa T, Yuasa T, et al. Immunophenotypical characterization of macrophages in rat bleomycin-induced scleroderma[J]. Vet Pathol, 2013, 50:76-85. doi:  10.1177/0300985812450718
    [48] Hone N, Donnelly C, Houk JB, et al. Macrophage Activation Syndrome in Scleroderma[J]. J Clin Rheumatol, 2017, 23:120-121. doi:  10.1097/RHU.0000000000000512
    • 相关文章
    • 施引文献
  • 资源附件(0)
  • 加载中
WeChat 点击查看大图
计量
  • 文章访问数:  200
  • HTML全文浏览量:  55
  • PDF下载量:  10
  • 被引次数: 0
出版历程
  • 收稿日期:  2018-03-08
  • 刊出日期:  2020-09-18

目录

    /

    返回文章
    返回
    友情链接: 国家卫生健康委员会 北京协和医院 中国医学科学院 学术不端检测系统 国际知识资源总库 中国知网 术语在线 中国全科医学
    地址：北京市东城区帅府园1号 北京协和医院老楼7号楼
    3层302室 《协和医学杂志》编辑部
    电话：010-69154261/4262
    E - mail：medj@pumch.cn
    mjpumch@126.com
    期刊网站版权所有：《协和医学杂志》编辑部
    京ICP备 11002662

    本系统由 北京仁和汇智信息技术有限公司 开发    百度统计

    x 关闭 永久关闭

    【温馨提醒】近日，《协和医学杂志》编辑部接到作者反映，有多名不法人员冒充期刊编辑发送见刊通知，鼓动作者添加微信，从而骗取版面费的行为。特提醒您，本刊与作者联系的方式均为邮件通知或电话，稿件进度通知邮箱为：mjpumch@126.com，编辑部电话为：010-69154261，请提高警惕，谨防上当受骗！如有任何疑问，请致电编辑部核实。谢谢！