Volume 13 Issue 2
Mar.  2022
Turn off MathJax
Article Contents
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

Risk Factors and Pathogenesis of the Recurrence of Psoriasis

doi: 10.12290/xhyxzz.2021-0367
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
  • Corresponding author: JIN Hongzhong, E-mail: jinhongzhong@263.net
  • Received Date: 2021-05-01
  • Accepted Date: 2021-07-29
  • Available Online: 2022-01-12
  • Publish Date: 2022-03-30
  • Psoriasis is a kind of chronic recurrent disease, which is easy to recur and protract. It has a severe impact on the life quality of patients. There are multiple factors for the relapse of psoriasis, such as stress, environment, life-style, endocrine and so on. The immunological mechanism of the recurrence of psoriasis is complex. Tissue-resident memory T cells (TRM) may play an important role in the immunological memory of psoriasis. To define the risk factors and the potential pathogenesis of the recurrence of psoriasis can provide basis for the clinical prevention of recurrence and aggravation of psoriasis. To block the function of TRM might open new avenues for preventing the recurrence of psoriasis.
  • loading
  • [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

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (1344) PDF downloads(154) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return