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中华妇幼临床医学杂志(电子版) ›› 2017, Vol. 13 ›› Issue (02) : 222 -225. doi: 10.3877/cma.j.issn.1673-5250.2017.02.019

所属专题: 文献

综述

白细胞介素-17及-35在子痫前期发病机制的研究进展
彭琦1   
  1. 1. 225001 江苏省扬州大学临床医学院妇产科;225200 江苏省扬州市江都人民医院妇产科
    2. 225001 江苏省扬州大学临床医学院妇产科
  • 收稿日期:2016-11-06 修回日期:2017-01-11 出版日期:2017-04-01

Research progress of interleukin-17 and -35 in pre-eclampsia

Qi Peng1   

  1. 1. Department of Obstetrics and Gynecology, Clinical College, Yangzhou University, Yangzhou 225001, Jiangsu Province, China; Department of Obstetrics and Gynecology, Jiangdu District People′s Hospital, Jiangdu 225200, Jiangsu Province, China
    2. Department of Obstetrics and Gynecology, Clinical College, Yangzhou University, Yangzhou 225001, Jiangsu Province, China
  • Received:2016-11-06 Revised:2017-01-11 Published:2017-04-01
  • About author:
    Corresponding author: Lu Dan, Email:
引用本文:

彭琦. 白细胞介素-17及-35在子痫前期发病机制的研究进展[J]. 中华妇幼临床医学杂志(电子版), 2017, 13(02): 222-225.

Qi Peng. Research progress of interleukin-17 and -35 in pre-eclampsia[J]. Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition), 2017, 13(02): 222-225.

子痫前期(PE)是导致孕产妇和围生儿患病率和死亡率增高的主要原因之一。临床对于PE的发病机制迄今尚未阐明。近年研究结果显示,PE与母-胎免疫耐受失衡关系密切,发生PE时,机体白细胞介素(IL)-17表达上调,而IL-35表达下调,辅助性T细胞(Th)17与调节性T细胞(Treg)的免疫平衡(Th17/Treg)出现偏移。笔者拟就IL-17及-35的结构、生理功能及其在PE发病机制中作用的最新研究进展进行综述。

Pre-eclampsia (PE) is one of important disorders that significantly contribute to the enhancement of maternal and neonatal mortality. The causes and mechanisms of PE are not fully clarified so far. In recent years, it has been shown by studies that PE is closely related to the imbalance of maternal-fetal immune tolerance. The expression of interleukin (IL)-17 is up-regulated, while the expression of IL-35 is down-regulated, and the immune balance of helper T cell (Th) 17 and regulatory T cell (Treg) is deviated in PE. The structures and functions of IL-17 and IL-35, and roles in the nosogenesis of PE are reviewed in this paper.

[1]
谢幸, 苟文丽. 妇产科学. 8版[M]. 北京: 人民卫生出版社, 2013: 64-71.
[2]
Laresgoiti-Servitje E. A leading role for the immune system in the pathophysiology of preeclampsia[J]. J Leukoc Biol, 2013, 94(2): 247-257.
[3]
Darmochwal-Kolarz D, Kludka-Sternik M, Tabarkiewicz J, et al. The predominance of Th17 lymphocytes and decreased number and function of Treg cells in preeclampsia[J]. J Reprod Immunol, 2012, 93(2): 75-81.
[4]
Yao Z, Fanslow WC, Seldin MF, et al. Herpesvirus Saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor[J]. Immunity, 1995, 3(6): 811-821.
[5]
Gu C, Wu L, Li X. IL-17 family: cytokines, receptors and signaling[J]. Cytokine, 2013, 64(2): 477-485.
[6]
Cornelius DC, Hogg JP, Scott J, et al. Administration of interleukin-17 soluble receptor C suppresses TH17 cells, oxidative stress, and hypertension in response to placental ischemia during pregnancy[J]. Hypertension, 2013, 62(6): 1068-1073.
[7]
Cornelius DC, Lamarca B. TH17- and IL-17- mediated autoantibodies and placental oxidative stress play a role in the pathophysiology of pre-eclampsia[J]. Minerva Ginecol, 2014, 66(3): 243-249.
[8]
Saifi B, Rezaee SA, Tajik N, et al. Th17 cells and related cytokines in unexplained recurrent spontaneous miscarriage at the implantation window[J]. Reprod Biomed Online, 2014, 29(4): 481-489.
[9]
汪勤, 赵春辉, 夏良萍, 等. 重度子痫前期患者外周血Th17和Treg细胞及相关细胞因子的表达及意义[J]. 检验医学与临床, 2015, 12(20): 3040-3043.
[10]
Toldi G, Rigó J Jr, Stenczer B, et al. Increased prevalence of IL-17-producing peripheral blood lymphocytes in pre-eclampsia[J]. Am J Reprod Immunol, 2011, 66(3): 223-229.
[11]
Devergne O, Birkenbach M, Kieff E. Epstein-Barr virus-induced gene 3 and the p35 subunit of interleukin 12 form a novel heterodimeric hematopoietin[J]. Proc Natl Acad Sci USA, 1997, 94(22): 12041-12046.
[12]
Collison LW, Workman CJ, Kuo TT, et al. The inhibitory cytokine IL-35 contributes to regulatory T-cell function[J]. Nature, 2007, 450(7169): 566-569.
[13]
Niedbala W, Wei XQ, Cai B, et al. IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells[J]. Eur J Immunol, 2007, 37(11): 3021-3029.
[14]
Olson BM, Sullivan JA, Burlingham WJ. Interleukin 35: a key mediator of suppression and the propagation of infectious tolerance[J]. Front Immunol, 2013, 4: 315.
[15]
Collison LW, Delgoffe GM, Guy CS, et al. The composition and signaling of the IL-35 receptor are unconventional[J]. Nat Immunol, 2012, 13(3): 290-299.
[16]
Aparicio-Siegmund S, Moll JM, Lokau J, et al. Recombinant p35 from bacteria can form interleukin (IL-)12, but not IL-35[J]. PLoS One, 2014, 9(9): e107990.
[17]
Jin E, Wang C, Hu Q, et al. The regular distribution and expression pattern of immunosuppressive cytokine IL-35 in mouse uterus during early pregnancy[J]. Rom J Morphol Embryol, 2014, 55(4): 1353-1361.
[18]
Yue CY, Zhang B, Ying CM. Elevated serum level of IL-35 associated with the maintenance of maternal-fetal immune tolerance in normal pregnancy[J]. PLoS One, 2015, 10(6): e0128219.
[19]
潘秀和, 彭笑, 高巧艳, 等. IL-35在感染、炎症与自身免疫性疾病中的作用[J]. 中华微生物学和免疫学杂志, 2015, 35(3): 237-240.
[20]
Cao W, Wang X, Chen T, et al. The Expression of Notch/Notch ligand, IL-35, IL-17, and Th17/Treg in preeclampsia[J]. Dis Markers, 2015, 2015: 316182.
[21]
闫永嘉, 何向辉. IL-35结构功能及其调控Treg细胞免疫抑制功能的研究进展[J]. 天津医药, 2014, 42(12): 1243-1245.
[22]
Harrington LE, Hatton RD, Mangan PR, et al. Interleukin 17-producing CD4effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages[J]. Nat Immunol, 2005, 6(11): 1123-1132.
[23]
Park H, Li Z, Yang XO, et al. A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17[J]. Nat Immunol, 2005, 6(11): 1133-1141.
[24]
Sakaguchi S, Sakaguchi N, Asano M, et al. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases[J]. J Immunol, 1995, 155(3): 1151-1164.
[25]
Schumacher A, Wafula PO, Teles A, et al. Blockage of heme oxygenase-1 abrogates the protective effect of regulatory T cells on murine pregnancy and promotes the maturation of dendritic cells[J]. PLoS One, 2012, 7(8): e42301.
[26]
魏志霞, 杨海澜, 韩方. Foxp3和RORγt基因在子痫前期患者外周血单个核细胞中的表达[J]. 中华妇产科杂志, 2013, 48(3): 204-206.
[27]
Mosmann TR, Coffman RL. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties[J]. Annu Rev Immunol, 1989, 7: 145-173.
[28]
Vargas-Rojas MI, Solleiro-Villavicencio H, Soto-Vega E. Th1, Th2, Th17 and Treg levels in umbilical cord blood in preeclampsia[J]. J Matern Fetal Neonatal Med, 2016, 29(10): 1642-1645.
[29]
Talaat RM, Mohamed SF, Bassyouni IH, et al. Th1/Th2/Th17/Treg cytokine imbalance in systemic lupus erythematosus (SLE) patients: correlation with disease activity[J]. Cytokine, 2015, 72(2): 146-153.
[30]
尹雪, 任秀敏, 刘春苗, 等. 变应性鼻炎患者IL-35对于Treg/Th17细胞平衡的调控作用[J]. 临床耳鼻喉头颈外科杂志, 2016, 30(3): 213-216.
[31]
Martin JC, Baeten DL, Josien R. Emerging role of IL-17 and Th17 cells in systemic lupus erythematosus[J]. Clin Immunol, 2014, 154(1): 1-12.
[32]
Papp KA, Langley RG, Sigurgeirsson B, et al. Efficacy and safety of secukinumab in the treatment of moderate-to-severe plaque psoriasis: a randomized, double-blind, placebo-controlled phase Ⅱ dose-ranging study[J]. Br J Dermatol, 2013, 168 (2): 412-421.
[33]
Li HC, Zhang YX, Liu Y, et al. Effect of IL-17 monoclonal antibody secukinumab combined with IL-35 blockade of Notch signaling pathway on the invasive capability of hepatoma cells[J]. Genet Mol Res, 2016, 15(2): 238-242.
[34]
Long J, Zhang X, Wen M, et al. IL-35 over-expression increases apoptosis sensitivity and suppresses cell growth in human cancer cells[J]. Biochem Biophys Res Commun, 2013, 430(1): 364-369.
[35]
Nakano S, Morimoto S, Suzuki S, et al. Immunoregulatory role of IL-35 in T cells of patients with rheumatoid arthritis[J]. Rheumatology (Oxford), 2015, 54 (8): 1498-1506.
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