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

银屑病复发的危险因素及机制

刘晓涵 晋红中

刘晓涵, 晋红中. 银屑病复发的危险因素及机制[J]. 协和医学杂志, 2022, 13(2): 308-314. doi: 10.12290/xhyxzz.2021-0367
引用本文: 刘晓涵, 晋红中. 银屑病复发的危险因素及机制[J]. 协和医学杂志, 2022, 13(2): 308-314. doi: 10.12290/xhyxzz.2021-0367
LIU Xiaohan, JIN Hongzhong. Risk Factors and Pathogenesis of the Recurrence of Psoriasis[J]. Medical Journal of Peking Union Medical College Hospital, 2022, 13(2): 308-314. doi: 10.12290/xhyxzz.2021-0367
Citation: LIU Xiaohan, JIN Hongzhong. Risk Factors and Pathogenesis of the Recurrence of Psoriasis[J]. Medical Journal of Peking Union Medical College Hospital, 2022, 13(2): 308-314. doi: 10.12290/xhyxzz.2021-0367

银屑病复发的危险因素及机制

doi: 10.12290/xhyxzz.2021-0367
基金项目: 

国家自然科学基金面上项目 81773331

国家重点研发计划罕见病临床队列研究 2016YFC0901500

中国医学科学院医学与健康科技创新工程 2021-I2M-1-059

详细信息
    通讯作者:

    晋红中,E-mail:jinhongzhong@263.net

  • 中图分类号: R758.63

Risk Factors and Pathogenesis of the Recurrence of Psoriasis

Funds: 

General Program of National Natural Science Foundation of China 81773331

National Key Research and Development Program of China 2016YFC0901500

CAMS Innovation Fund for Medical Sciences 2021-I2M-1-059

More Information
  • 摘要: 银屑病是一种慢性复发性疾病, 易反复发作, 迁延不愈, 严重影响患者的生活质量。银屑病复发的诱因多样, 包括精神压力、环境、生活方式、内分泌等多种因素。银屑病复发的免疫机制复杂, 组织常驻记忆T细胞可能在银屑病的免疫记忆中发挥重要作用。明确银屑病复发的危险因素及机制, 可为临床上预防和治疗银屑病反复发作及病情加重提供依据。阻断组织常驻记忆T细胞功能可能为预防银屑病复发的新思路。
    作者贡献:刘晓涵负责文献资料收集、分析及论文撰写;晋红中负责论文构思及审校。
    利益冲突:所有作者均声明不存在利益冲突
  • [1] Georgescu SR, Tampa M, Caruntu C, et al. Advances in Understanding the Immunological Pathways in Psoriasis[J]. Int J Mol Sci, 2019, 20: 739. doi:  10.3390/ijms20030739
    [2] Luo Y, Ru Y, Sun X, et al. Characteristics of psoriasis vulgaris in China: a prospective cohort study protocol[J]. Ann Transl Med, 2019, 7: 694. doi:  10.21037/atm.2019.10.46
    [3] Carey W, Glazer S, Gottlieb AB, et al. Relapse, rebound, and psoriasis adverse events: an advisory group report[J]. J Am Acad Dermatol, 2006, 54: S171-S181. doi:  10.1016/j.jaad.2005.10.029
    [4] Kamaria M, Liao W, Koo JY. How Long Does the Benefit of Biologics Last? An Update on Time To Relapse and Potential for Rebound of Biologic Agents for Psoriasis[J]. Psoriasis Forum, 2010, 16: 36-42.
    [5] Florek AG, Wang CJ, Armstrong AW. Treatment prefer-ences and treatment satisfaction among psoriasis patients: a systematic review[J]. Arch Dermatol Res, 2018, 310: 271-319. doi:  10.1007/s00403-018-1808-x
    [6] Stewart TJ, Tong W, Whitfeld MJ. The associations between psychological stress and psoriasis: a systematic review[J]. Int J Dermatol, 2018, 57: 1275-1282. doi:  10.1111/ijd.13956
    [7] Vegas O, Poligone B, Blackcloud P, et al. Chronic social stress Ameliorates psoriasiform dermatitis through upregula-tion of the Hypothalamic-Pituitary-Adrenal axis[J]. Brain Behav Immun, 2018, 68: 238-247. doi:  10.1016/j.bbi.2017.10.022
    [8] Evers AW, Verhoeven EW, Kraaimaat FW, et al. How stress gets under the skin: cortisol and stress reactivity in psoriasis[J]. Br J Dermatol, 2010, 163: 986-991. doi:  10.1111/j.1365-2133.2010.09984.x
    [9] Zhang Y, Zhang H, Jiang B, et al. A promising thera-peutic target for psoriasis: Neuropeptides in human skin[J]. Int Immunopharmacol, 2020, 87: 106755. doi:  10.1016/j.intimp.2020.106755
    [10] Wang Y, Li P, Zhang L, et al. Stress aggravates and prolongs imiquimod-induced psoriasis-like epidermal hyperplasis and IL-1β/IL-23p40 production[J]. J Leukoc Biol, 2020, 108: 267-281. doi:  10.1002/JLB.3MA0320-363RR
    [11] Ertle CM, Rommel FR, Tumala S, et al. New Pathways for the Skin's Stress Response: The Cholinergic Neurope-ptide SLURP-1 Can Activate Mast Cells and Alter Cytokine Production in Mice[J]. Front Immunol, 2021, 12: 631881. doi:  10.3389/fimmu.2021.631881
    [12] Buske-Kirschbaum A, Kern S, Ebrecht M, et al. Altered distribution of leukocyte subsets and cytokine production in response to acute psychosocial stress in patients with psoriasis vulgaris[J]. Brain Behav Immun, 2007, 21: 92-99. doi:  10.1016/j.bbi.2006.03.006
    [13] Pezzolo E, Naldi L. The relationship between smoking, psoriasis and psoriatic arthritis[J]. Expert Rev Clin Immunol, 2019, 15: 41-48. doi:  10.1080/1744666X.2019.1543591
    [14] Huang ZZ, Xu Y, Xu M, et al. Artesunate alleviates imiquimod-induced psoriasis-like dermatitis in BALB/c mice[J]. Int Immunopharmacol, 2019, 75: 105817. doi:  10.1016/j.intimp.2019.105817
    [15] Gazel U, Ayan G, Solmaz D, et al. The impact of smoking on prevalence of psoriasis and psoriatic arthritis[J]. Rheumatology (Oxford), 2020, 59: 2695-2710. doi:  10.1093/rheumatology/keaa179
    [16] Al-Jefri K, Newbury-Birch D, Muirhead CR, et al. High prevalence of alcohol use disorders in patients with inflammatory skin diseases[J]. Br J Dermatol, 2017, 177: 837-844. doi:  10.1111/bjd.15497
    [17] Dai YX, Wang SC, Chou YJ, et al. Smoking, but not alcohol, is associated with risk of psoriasis in a Taiwanese population-based cohort study[J]. J Am Acad Dermatol, 2019, 80: 727-734. doi:  10.1016/j.jaad.2018.11.015
    [18] Svanström C, Lonne-Rahm SB, Nordlind K. Psoriasis and alcohol[J]. Psoriasis (Auckl), 2019, 9: 75-79.
    [19] Kim SK, Choe JY, Park KY. Ethanol Augments Monoso-dium Urate-Induced NLRP3 Inflammasome Activation via Regulation of AhR and TXNIP in Human Macrophages[J]. Yonsei Med J, 2020, 61: 533-541. doi:  10.3349/ymj.2020.61.6.533
    [20] Vasseur P, Pohin M, Gisclard C, et al. Chronic Alcohol Consumption Exacerbates the Severity of Psoriasiform Dermatitis in Mice[J]. Alcohol Clin Exp Res, 2020, 44: 1728-1733. doi:  10.1111/acer.14400
    [21] Irwin MR. Sleep and inflammation: partners in sickness and in health[J]. Nat Rev Immunol, 2019, 19: 702-715. doi:  10.1038/s41577-019-0190-z
    [22] Yang H, Li X, Zhang L, et al. Immunomodulatory effects of sleep deprivation at different timing of psoriasiform process on skin inflammation[J]. Biochem Biophys Res Commun, 2019, 513: 452-459. doi:  10.1016/j.bbrc.2019.03.185
    [23] Afifi L, Danesh MJ, Lee KM, et al. Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey[J]. Dermatol Ther (Heidelb), 2017, 7: 227-242. doi:  10.1007/s13555-017-0183-4
    [24] Kanda N, Hoashi T, Saeki H. Nutrition and Psoriasis[J]. Int J Mol Sci, 2020, 21: 5405. doi:  10.3390/ijms21155405
    [25] Castaldo G, Rastrelli L, Galdo G, et al. Aggressive weight-loss program with a ketogenic induction phase for the treatment of chronic plaque psoriasis: A proof-of-concept, single-arm, open-label clinical trial[J]. Nutrition, 2020, 74: 110757. doi:  10.1016/j.nut.2020.110757
    [26] Castaldo G, Pagano I, Grimaldi M, et al. Effect of Very-Low-Calorie Ketogenic Diet on Psoriasis Patients: A Nuclear Magnetic Resonance-Based Metabolomic Study[J]. J Proteome Res, 2020, 20: 1509-1521.
    [27] Ji YZ, Liu SR. Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechan-isms[J]. Biosci Rep, 2019, 39: BSR20193266. doi:  10.1042/BSR20193266
    [28] Raychaudhuri SP, Jiang WY, Raychaudhuri SK. Revisiting the Koebner phenomenon: role of NGF and its receptor system in the pathogenesis of psoriasis[J]. Am J Pathol, 2008, 172: 961-971. doi:  10.2353/ajpath.2008.070710
    [29] Gregorio J, Meller S, Conrad C, et al. Plasmacytoid dendritic cells sense skin injury and promote wound healing through type Ⅰ interferons[J]. J Exp Med, 2010, 207: 2921-2930. doi:  10.1084/jem.20101102
    [30] Zhang LJ, Sen GL, Ward NL, et al. Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury[J]. Immunity, 2016, 45: 119-130. doi:  10.1016/j.immuni.2016.06.021
    [31] Thorleifsdottir RH, Eysteinsdóttir JH, Olafsson JH, et al. Throat Infections are Associated with Exacerbation in a Substantial Proportion of Patients with Chronic Plaque Psoriasis[J]. Acta Derm Venereol, 2016, 96: 788-791.
    [32] Rademaker M, Agnew K, Anagnostou N, et al. Psoriasis and infection. A clinical practice narrative[J]. Australas J Dermatol, 2019, 60: 91-98. doi:  10.1111/ajd.12895
    [33] Alsubeeh NA, Alsharafi AA, Ahamed SS, et al. Treatment Adherence Among Patients with Five Dermatological Diseases and Four Treatment Types- a Cross-Sectional Study[J]. Patient Prefer Adherence, 2019, 13: 2029-2038. doi:  10.2147/PPA.S230921
    [34] Choi JW, Kim BR, Youn SW. Adherence to Topical Therapies for the Treatment of Psoriasis: Surveys of Physicians and Patients[J]. Ann Dermatol, 2017, 29: 559-564. doi:  10.5021/ad.2017.29.5.559
    [35] Okwundu N, Cardwell L, Cline A, et al. Is topical treatment effective for psoriasis in patients who failed topical treatment?[J]. J Dermatolog Treat, 2021, 32: 41-44. doi:  10.1080/09546634.2019.1617830
    [36] Wang W, Qiu Y, Zhao F, et al. Poor medication adherence in patients with psoriasis and a successful intervention[J]. J Dermatolog Treat, 2019, 30: 525-528. doi:  10.1080/09546634.2018.1476652
    [37] Balak DM, Hajdarbegovic E. Drug-induced psoriasis: clinical perspectives[J]. Psoriasis (Auckl), 2017, 7: 87-94.
    [38] Kamiya K, Kishimoto M, Sugai J, et al. Risk Factors for the Development of Psoriasis[J]. Int J Mol Sci, 2019, 20: 4347. doi:  10.3390/ijms20184347
    [39] Boyd AS, Morris LF, Phillips CM, et al. Psoriasis and pregnancy: hormone and immune system interaction[J]. Int J Dermatol, 1996, 35: 169-172. doi:  10.1111/j.1365-4362.1996.tb01632.x
    [40] Murase JE, Chan KK, Garite TJ, et al. Hormonal effect on psoriasis in pregnancy and post partum[J]. Arch Dermatol, 2005, 141: 601-606.
    [41] Lin X, Huang T. Impact of pregnancy and oestrogen on psoriasis and potential therapeutic use of selective oestrogen receptor modulators for psoriasis[J]. J Eur Acad Dermatol Venereol, 2016, 30: 1085-1091. doi:  10.1111/jdv.13661
    [42] Wang H, Wang Z, Rani PL, et al. Identification of PTPN22, ST6GAL1 and JAZF1 as psoriasis risk genes demonstrates shared pathogenesis between psoriasis and diabetes[J]. Exp Dermatol, 2017, 26: 1112-1117. doi:  10.1111/exd.13393
    [43] Jin Y, Zhang F, Yang S, et al. Combined effects of HLA-Cw6, body mass index and waist-hip ratio on psoriasis vulgaris in Chinese Han population[J]. J Dermatol Sci, 2008, 52: 123-129. doi:  10.1016/j.jdermsci.2008.04.016
    [44] Kim ES, Han K, Kim MK, et al. Impact of metabolic status on the incidence of psoriasis: a Korean nationwide cohort study[J]. Sci Rep, 2017, 7: 1989. doi:  10.1038/s41598-017-01983-y
    [45] Ferguson LD, Brown R, Celis-Morales C, et al. Associa-tion of central adiposity with psoriasis, psoriatic arthritis and rheumatoid arthritis: a cross-sectional study of the UK Biobank[J]. Rheumatology (Oxford), 2019, 58: 2137-2142. doi:  10.1093/rheumatology/kez192
    [46] Brazzelli V, Maffioli P, Bolcato V, et al. Psoriasis and Diabetes, a Dangerous Association: Evaluation of Insulin Resistance, Lipid Abnormalities, and Cardiovascular Risk Biomarkers[J]. Front Med (Lausanne), 2021, 8: 605691.
    [47] Kanemaru K, Matsuyuki A, Nakamura Y, et al. Obesity exacerbates imiquimod-induced psoriasis-like epidermal hyperplasia and interleukin-17 and interleukin-22 production in mice[J]. Exp Dermatol, 2015, 24: 436-442. doi:  10.1111/exd.12691
    [48] Pan Y, Tian T, Park CO, et al. Survival of tissue-resident memory T cells requires exogenous lipid uptake and metabolism[J]. Nature, 2017, 543: 252-256. doi:  10.1038/nature21379
    [49] Zhang JZ, Ding Y, Xiang F, et al. Effectiveness and safety of different doses of pioglitazone in psoriasis: a meta-analysis of randomized controlled trials[J]. Chin Med J (Engl), 2020, 133: 444-451. doi:  10.1097/CM9.0000000000000642
    [50] Xu X, Lin L, Chen P, et al. Treatment with liraglutide, a glucagon-like peptide-1 analogue, improves effectively the skin lesions of psoriasis patients with type 2 diabetes: A prospective cohort study[J]. Diabetes Res Clin Pract, 2019, 150: 167-173. doi:  10.1016/j.diabres.2019.03.002
    [51] Lynch M, Malara A, Timoney I, et al. Sitagliptin and Narrow-Band Ultraviolet-B for Moderate Psoriasis (DINUP): A Randomised Controlled Clinical Trial[J]. Dermatology, 2021: 1-8.
    [52] Tsuji G, Hashimoto-Hachiya A, Yen VH, et al. Metformin inhibits IL-1β secretion via impairment of NLRP3 inflammasome in keratinocytes: implications for preventing the development of psoriasis[J]. Cell Death Discov, 2020, 6: 11.
    [53] Matos TR, O'Malley JT, Lowry EL, et al. Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing αβ T cell clones[J]. J Clin Invest, 2017, 127: 4031-4041. doi:  10.1172/JCI93396
    [54] Vo S, Watanabe R, Koguchi-Yoshioka H, et al. CD8 resident memory T cells with interleukin 17A-producing potential are accumulated in disease-naïve nonlesional sites of psoriasis possibly in correlation with disease duration[J]. Br J Dermatol, 2019, 181: 410-412. doi:  10.1111/bjd.17748
    [55] Cheuk S, Wikén M, Blomqvist L, et al. Epidermal Th22 and Tc17 cells form a localized disease memory in clinically healed psoriasis[J]. J Immunol, 2014, 192: 3111-3120. doi:  10.4049/jimmunol.1302313
    [56] Kurihara K, Fujiyama T, Phadungsaksawasdi P, et al. Significance of IL-17A-producing CD8(+)CD103(+) skin resident memory T cells in psoriasis lesion and their possible relationship to clinical course[J]. J Dermatol Sci, 2019, 95: 21-27. doi:  10.1016/j.jdermsci.2019.06.002
    [57] Bromley SK, Akbaba H, Mani V, et al. CD49a Regulates Cutaneous Resident Memory CD8(+) T Cell Persistence and Response[J]. Cell Rep, 2020, 32: 108085. doi:  10.1016/j.celrep.2020.108085
    [58] Fenix K, Wijesundara DK, Cowin AJ, et al. Immunolo-gical Memory in Imiquimod-Induced Murine Model of Psoriasiform Dermatitis[J]. Int J Mol Sci, 2020, 21: 7228. doi:  10.3390/ijms21197228
    [59] Mackay LK, Braun A, Macleod BL, et al. Cutting edge: CD69 interference with sphingosine-1-phosphate receptor function regulates peripheral T cell retention[J]. J Immunol, 2015, 194: 2059-2063. doi:  10.4049/jimmunol.1402256
    [60] Fukui T, Fukaya T, Uto T, et al. Pivotal role of CD103 in the development of psoriasiform dermatitis[J]. Sci Rep, 2020, 10: 8371. doi:  10.1038/s41598-020-65355-9
    [61] Chen Y, Yan Y, Liu H, et al. Dihydroartemisinin amelio-rates psoriatic skin inflammation and its relapse by diminishing CD8+ T-cell memory in wild-type and humanized mice[J]. Theranostics, 2020, 10: 10466-10482. doi:  10.7150/thno.45211
    [62] Heier I, Søyland E, Krogstad AL, et al. Sun exposure rapidly reduces plasmacytoid dendritic cells and inflammatory dermal dendritic cells in psoriatic skin[J]. Br J Dermatol, 2011, 165: 792-801. doi:  10.1111/j.1365-2133.2011.10430.x
    [63] Malaviya R, Sun Y, Tan JK, et al. Etanercept induces apoptosis of dermal dendritic cells in psoriatic plaques of responding patients[J]. J Am Acad Dermatol, 2006, 55: 590-597. doi:  10.1016/j.jaad.2006.05.004
    [64] Günther C, Blau K, Förster U, et al. Reduction of inflammatory slan (6-sulfo LacNAc) dendritic cells in psoriatic skin of patients treated with etanercept[J]. Exp Dermatol, 2013, 22: 535-540. doi:  10.1111/exd.12190
    [65] Naik S, Larsen SB, Gomez NC, et al. Inflammatory memory sensitizes skin epithelial stem cells to tissue damage[J]. Nature, 2017, 550: 475-480. doi:  10.1038/nature24271
  • 加载中
计量
  • 文章访问数:  1309
  • HTML全文浏览量:  124
  • PDF下载量:  152
  • 被引次数: 0
出版历程
  • 收稿日期:  2021-05-01
  • 录用日期:  2021-07-29
  • 网络出版日期:  2022-01-12
  • 刊出日期:  2022-03-30

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!