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Th2相关炎症因子在湿疹发病中的作用机制

朱聪聪,  潘会君,  朱全刚

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文章导航 > 药学实践与服务  > 2019 >  37(1): 9-13
朱聪聪, 潘会君, 朱全刚. Th2相关炎症因子在湿疹发病中的作用机制[J]. 药学实践与服务, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
引用本文: 朱聪聪, 潘会君, 朱全刚. Th2相关炎症因子在湿疹发病中的作用机制[J]. 药学实践与服务, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
shu
ZHU Congcong, PAN Huijun, ZHU Quangang. Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
Citation: ZHU Congcong, PAN Huijun, ZHU Quangang. Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
shu

Th2相关炎症因子在湿疹发病中的作用机制

doi: 10.3969/j.issn.1006-0111.2019.01.003
  • 1.

    上海中医药大学附属岳阳中西医结合医院药学研究室, 上海 200437;上海市皮肤病医院药剂科, 上海 200443

  • 2.

    上海市皮肤病医院药剂科, 上海 200443

基金项目: 上海市科委资助项目（17401901800）

Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema

  • 1.

    Department of Pharmacy Laboratory, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China;Department of Pharmacy, Shanghai Dermatology Hospital, Shanghai 200443, China

  • 2.

    Department of Pharmacy, Shanghai Dermatology Hospital, Shanghai 200443, China

  • 摘要: 湿疹是临床常见的炎症性皮肤病，具有剧烈瘙痒、反复发作等特点。其病因复杂，包括多种内、外因素相互作用。主要发病机制与Th2免疫应答失衡有关，相关的炎症因子更是发挥十分重要的作用。上皮衍生因子胸腺基质淋巴细胞生成素以及白介素-33（IL-33）能够引发Th2免疫失衡，促进IL-4、IL-5、IL-13等炎症因子分泌，后者进一步诱导嗜酸性粒细胞增多、IgE生成。综述Th2相关炎症因子在湿疹发病中的作用机制，对湿疹治疗具有重要意义。
    Abstract: Eczema is a common clinical inflammatory skin disease characterized by severe itching and recurrent attacks.Its etiology is complex, including a variety of internal and external factors.The main mechanism is related to the imbalance of Th2 immune response, and related inflammatory factors play an important role.Epithelial-derived factor like thymic stromal lymphopoietin and interleukin-33 could trigger Th2 immune imbalance and promote the secretion of type inflammatory factors such as interleukin-4, interleukin-5, and interleukin-13.These inflammatory factors will further induce eosinophilic granulocytosis and IgE formation.In this paper, the research progress of mechanism of type 2 related inflammatory factors in eczema were reviewed, which provided the great significance for treatment.
  • [1] DECKERS I A,MCLEAN S,LINSSEN S,et al.Investigating international time trends in the incidence and prevalence of atopic eczema 1990-2010:a systematic review of epidemiological studies[J].PLoS ONE,2012,7(7):e39803.
    [2] WEIDINGER S,NOVAK N.Atopic dermatitis[J].Lancet,2016,387(10023):1109-1122.
    [3] EYERICH K,NOVAK N.Immunology of atopic eczema:overcoming the Th1/Th2 paradigm.[J].Allergy,2013,68(8):974-982.
    [4] ESAKI H,BRUNNER P M,RENERT-YUVAL Y,et al.Early-onset pediatric atopic dermatitis is Th2 but also Th17 polarized in skin[J].J Allergy Clin Immunol,2016,138(6):1639-1651.
    [5] EYERICH K,EYERICH S.Th22 cells in allergic disease[J].Allergo J Int,2015,24(1):1-7.
    [6] LIU Y J,SOUMELIS V,WATANABE N,et al.TSLP:an epithelial cell cytokine that regulates T cell differentiation by conditioning dendritic cell maturation[J].Annu Rev Immunol,2007,25:193-219.
    [7] SCHMITZ J,OWYANG A,OLDHAM E,et al.IL-33,an Interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines[J].Immunity,2005,23(5):479-490.
    [8] HAYAKAWA H,HAYAKAWA M,KUME A,et al.Soluble ST2 blocks interleukin-33 signaling in allergic airway inflammation[J]. J Biol Chem,2007,282(36):26369-26380.
    [9] TAKAHASHI N,SUGAYA M,SUGA H,et al.Thymic stromal chemokine TSLP acts through Th2 cytokine production to induce cutaneous t-cell lymphoma[J].Cancer Res,2016,76(21):6241-6252.
    [10] DOLGIN E.First eczema biologic debuts but price could restrict use[J].Nat Biotechnol,2017,35(5):391-392.
    [11] WANG X,JIANG X,YU X,et al.Cimifugin suppresses allergic inflammation by reducing epithelial derived initiative key factors via regulating tight junctions[J].J Cell Mol Med,2017,21(11):2926-2936.
    [12] CAYROL C,GIRARD J P.Interleukin-33(IL-33):A nuclear cytokine from the IL-1 family[J]. Nat Immunol,2018,281(1):154-168.
    [13] CAYROL C,DUVAL A,SCHMITT P,et al.Environmental allergens induce allergic inflammation through proteolytic maturation of IL-33[J].Nat Immunol,2018,19(4):375-385.
    [14] Ding W,Zou G L,Zhang W,et al.Interleukin-33:its emerging role in allergic diseases[J].Molecules,2018,23(7):1665.
    [15] CHEN W Y,TSAI T H,YANG J L,et al.Therapeutic strategies for targeting IL-33/ST2 signalling for the treatment of inflammatory diseases[J].Cell Physiol Biochem,2018,49(1):349-358.
    [16] DU H Y,FU H Y,LI D N,et al.The expression and regulation of interleukin-33 in human epidermal keratinocytes:a new mediator of atopic dermatitis and its possible signaling pathway[J].J Interferon Cytokine Res,2016,36(9):552-562.
    [17] RYU W I,LEE H,BAE H C et al.IL-33 down-regulates filaggrin expression by inducing STAT3 and ERK phosphorylation in human keratinocytes[J].J Dermatol Sci,2016,82(2):131-134.
    [18] DE SALVO C,,WANG X M,PASTORELLI L et al.IL-33 drives eosinophil infiltration and pathogenic type 2 helper T-cell immune responses leading to chronic experimental ileitis[J].Am J Pathol,2016,186(4):885-898.
    [19] LI C,MAILLET I,MACKOWIAK C,et al.Experimental atopic dermatitis depends on IL-33R signaling via MyD88 in dendritic cells[J].Cell Death Dis,2017,8(4):e2735.
    [20] PENG G,MU Z,CUI L,et al.Anti-IL-33 antibody has a therapeutic effect in an atopic dermatitis murine model induced by 2,4-dinitrochlorobenzene[J].Inflammation,2018,41(1):154-163.
    [21] JOHANSSON K,MALMHALL C,RAMOS-RAMÍREZ P,et al.Bone marrow type 2 innate lymphoid cells:a local source of interleukin-5 in interleukin-33-driven eosinophilia[J].Immunology,2018,153(2):268-278.
    [22] CAMELO A,ROSIGNOLI G,OHNE Y,et al.IL-33,IL-25,and TSLP induce a distinct phenotypic and activation profile in human type 2 innate lymphoid cells[J].Blood Adv,2017,1(10):577-589.
    [23] XU M,DONG C.IL-25 in allergic inflammation[J].Immunol Rev,2017,278(1):185-191.
    [24] GANDHI N A,BENNETT B L,GRAHAM N M,et al.Targeting key proximal drivers of type 2 inflammation in disease[J].Nat Rev Drug Discov,2016,15(1):35-50.
    [25] ROBINSON M J,PROUT M,MEARNS H,et al.IL-4 haploinsufficiency specifically impairs IgE responses against allergens in mice[J].J Immunol,2017,198(5):1815-1822.
    [26] HEIL P M,MAURER D,KLEIN B,et al.Omalizumab therapy in atopic dermatitis:depletion of IgE does not improve the clinical course-a randomized,placebo-controlled and double blind pilot study[J].JDDG,2010,8(12):990-998.
    [27] OLDHOFF J M,DARSOW U,WERFEL T,et al.Anti-IL-5 recombinant humanized monoclonal antibody (mepolizumab) for the treatment of atopic dermatitis[J].Allergy,2015,60(5):693-696.
    [28] ORTEGA H G,LIU MC,PAVORD I D,et al.Mepolizumab treatment in patients with severe eosinophilic asthma[J].New Engl J Med,2014,371(13):1198-1207..
    [29] CHANG H Y,NADEAU K C.IL-4Rα Inhibitor for Atopic Disease[J].Cell,2017,170(2):222.
    [30] THOMSON J,WERNHAM A G H,WILLIAMS H C.Long-term management of moderate-to-severe atopic dermatitis with dupilumab and concomitant topical corticosteroids (LIBERTY AD CHRONOS):a critical appraisal[J].Br J Dermatol,2018,178(4):897-902.
    [31] SZEGEDI K,VAN LIER A,RES P C,et al.House dust mite allergens Der f and Der p induce IL-31 production by blood-derived T cells from atopic dermatitis patients[J].Exp Dermatol,2018,27(4):393-395.
    [32] LEE M Y,SHIN E,KIM H et al.Interleukin-31,Interleukin-31RA,and OSMR expression levels in post-burn hypertrophic scars[J].J Pathol Transl Med,2018,52(5):307-313.
    [33] RAAP U,WICHMANN K,BRUDER M,et al.Correlation of IL-31 serum levels with severity of atopic dermatitis.[J].J Allergy Clin Immunol,2008,122(2):421-423.
    [34] NEIS M M,PETERS B,DREUW A,et al.Enhanced expression levels of IL-31 correlate with IL-4 and IL-13 in atopic and [KG3*9]allergic contact dermatitis[J].J Allergy Clin Immunol,2006,118(4):930-937.
    [35] CEVIKBAS F,WANG X,AKIYAMA T,et al.A sensory neuron-expressed IL-31 receptor mediates T helper cell-dependent itch:Involvement of TRPV1 and TRPA1[J].J Allergy Clin Immunol,2014,133(2):448-460.
    [36] ANDOH T,HARADA A,KURAISHI Y.Involvement of Leukotriene B4 released from keratinocytes in itch-associated response to intradermal interleukin-31 in mice[J].Acta Derm Venereol,2017,97(8):922-927.
    [37] NEMOTO O,FURUE M,NAKAGAWA H,et al.The first trial of CIM331,a humanized antihuman interleukin-31 receptor A antibody,in healthy volunteers and patients with atopic dermatitis to evaluate safety,tolerability and pharmacokinetics of a single dose in a randomized,double-blind,placebo-controlled study[J].Br J Dermatol,2016,174(2):296-304.
    [38] STANDER S,STEINHOFF M.Pathophysiology of pruritus in atopic dermatitis:an overview[J].Exp Dermatol,2002,11(1):12-24.
    [39] BAHALI A G,ONSUN N,SU O,et al.The relationship between pruritus and clinical variables in patients with psoriasis[J].An Bras Dermatol,2017,92(4):470-473.
    [40] ZEIDLER C,TSIANAKAS A,PEREIRA M,et al.Chronic prurigo of nodular type:a review[J].Acta Derm Venereol,2018,98(2):173-179.
    [41] KABASHIMA K,FURUE M,HANIFIN J M et al.Nemolizumab in patients with moderate-to-severe atopic dermatitis:Randomized,phase Ⅱ,long-term extension study[J].J Allergy Clin Immunol,2018,142(4):1121-1130.
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  • 收稿日期:  2018-09-28
  • 修回日期:  2018-11-20

Th2相关炎症因子在湿疹发病中的作用机制

doi: 10.3969/j.issn.1006-0111.2019.01.003
  • 1. 上海中医药大学附属岳阳中西医结合医院药学研究室, 上海 200437;上海市皮肤病医院药剂科, 上海 200443
  • 2. 上海市皮肤病医院药剂科, 上海 200443
    • 基金项目:  上海市科委资助项目（17401901800）
  • 收稿日期: 2018-09-28
  • 修回日期: 2018-11-20

摘要: 湿疹是临床常见的炎症性皮肤病，具有剧烈瘙痒、反复发作等特点。其病因复杂，包括多种内、外因素相互作用。主要发病机制与Th2免疫应答失衡有关，相关的炎症因子更是发挥十分重要的作用。上皮衍生因子胸腺基质淋巴细胞生成素以及白介素-33（IL-33）能够引发Th2免疫失衡，促进IL-4、IL-5、IL-13等炎症因子分泌，后者进一步诱导嗜酸性粒细胞增多、IgE生成。综述Th2相关炎症因子在湿疹发病中的作用机制，对湿疹治疗具有重要意义。

English Abstract

朱聪聪, 潘会君, 朱全刚. Th2相关炎症因子在湿疹发病中的作用机制[J]. 药学实践与服务, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
引用本文: 朱聪聪, 潘会君, 朱全刚. Th2相关炎症因子在湿疹发病中的作用机制[J]. 药学实践与服务, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
shu
ZHU Congcong, PAN Huijun, ZHU Quangang. Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
Citation: ZHU Congcong, PAN Huijun, ZHU Quangang. Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 9-13. doi: 10.3969/j.issn.1006-0111.2019.01.003
shu

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