Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema

ZHU Congcong; PAN Huijun; ZHU Quangang

doi:10.3969/j.issn.1006-0111.2019.01.003

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2019 > 37(1): 9-13

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

Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema

doi: 10.3969/j.issn.1006-0111.2019.01.003

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

Received Date: 2018-09-28
Rev Recd Date: 2018-11-20

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.
- eczema,
- inflammatory factor,
- TSLP,
- IL-4

References

[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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通讯作者: 陈斌, [email protected]

1.
沈阳化工大学材料科学与工程学院沈阳 110142

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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

Received Date: 2018-09-28

Rev Recd Date: 2018-11-20

Key words:

eczema /
inflammatory factor /
TSLP /
IL-4

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.

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Reference (41)

[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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Mechanism of Th2 related inflammatory factors in the pathogenesis of eczema

doi: 10.3969/j.issn.1006-0111.2019.01.003

Abstract

References

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通讯作者: 陈斌, [email protected]

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