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

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
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

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
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

More Information
  • 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。
    利益冲突  无
  • [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
  • 加载中
计量
  • 文章访问数:  184
  • HTML全文浏览量:  51
  • PDF下载量:  9
  • 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

    【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!