白癜风发病机制的研究进展
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摘要
白癜风是皮肤科常见的色素脱失性疾病,该病可发生于全身各部位,临床表现为边界清楚的乳白色斑片,主要分为节段性和非节段性。目前白癜风发病机制和病因尚不清楚,主要与遗传、免疫、氧化应激、黑素细胞自毁等多种因素密切相关,虽学说众多,但至今无任一学说能解释该疾病的发生。
Vitiligo is a common depigmentation disorder in the Dermatology Department. The disease can occur in all parts of the body. The clinical manifestations are milky white patches with clear boundaries, mainly divided into segmental and non-segmental. At present, the pathogenesis and etiology of vitiligo is still unclear, mainly related to genetic, immune, oxidative stress, self-destruction of melanocyte and other factors. Although there are many theories, but so far no theory can explain the occurrence of the disease.
Vitiligo is a common depigmentation disorder in the Dermatology Department. The disease can occur in all parts of the body. The clinical manifestations are milky white patches with clear boundaries, mainly divided into segmental and non-segmental. At present, the pathogenesis and etiology of vitiligo is still unclear, mainly related to genetic, immune, oxidative stress, self-destruction of melanocyte and other factors. Although there are many theories, but so far no theory can explain the occurrence of the disease.
引文
[1]Whitton ME,Ashcroft DM,Barrett CW,et al.Interventions for vitiligo:a Cochrane systematic review[J].British Journal of Dermatology,2006,25(1):41.
[2]Alkhateeb A,Fain PR,Thody A,et al.Epidemiology of vitiligo and associated autoimmune diseases in Caucasian probands and theirfamilies[J].Pigment Cell Res,2003,(16):208-214.
[3]Spritz RA.The genetics of generalized vitiligo:Autoimmune pathways and an inverse relationship with malignant melanoma[J].Genome Med,2010,19(2):78.
[4]Wang P,Li Y,Nie H,et al.The changes of gene expression profiling between segmental vitiligo,generalized vitiligo and healthy individual[J].J Dermatol Sci,2016,(84):40-9.
[5]?ahmatova L,Tankov S,Prans E,et al.MicroRNA-155 is Dysregulated in the Skin of Patients withVitiligo and Inhibits Melanogenesis-associated Genes in Melanocytesand Keratinocytes[J].Acta Derm Venereol,2016,(96):742-747.
[6]Traks T,Keermann M,Karelson M,et al.Polymorphisms in Tolllike receptor genes are associated withvitiligo[J].Front Genet,2015,(6):278.
[7]Le Poole IC,van den Wijngaard RM,Westerhof W,et al.Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance[J].Am J Pathol,1996,(148):1219-1228.
[8]Allard EL,Hardy MP,Leignadier J,et al.Overexpression of IL-21promotes massive CD8+memory T cell accumulation[J].Eur J Immunol,2007,(37):3069-3077.
[9]Harris JE,Harris TH,Weninger W,et al.A mouse model of vitiligo with focused epidermal depigmentation requires IFN-g for autoreactive CD8+T-cell accumulation in the skin[J].J Invest Dermatol,2012,(132):1869-1876.
[10]李博为,李舒丽,杨钰琪,等.白癜风免疫微环境对黑素细胞CX-CL10表达的影响[J].中国麻风皮肤病杂志,2017,33(1):8-11.
[11]Singh RK,Lee KM,Vujkovic-Cvijin I,et al.The role of IL-17 in vitiligo:A review[J].Autoimmun Rev,2016,(15):397-404.
[12]Zhou L,Shi YL,Li K,et al.Increased circulating Th17 cells and elevated serum levels of TGF-beta and IL-21 are correlated with human non-segmental vitiligo development Pigment Cell Melanoma[J].Res,2015,(28):324-329.
[13]Bhardwaj S,Rani S,Srivastava N,et al.Increased systemic and epidermal levels of IL-17A and IL-1β promotes progression of non-segmental vitiligo[J].Cytokine,2017,(91):153-161.
[14]Naughton GK,Eisinger M,Bystryn JC.Antibodies to normal human melanocytes in vitiligo[J].J Exp Med,1983,158(1):246-251.
[15]Westerhof W,Manini P,Napolitano A,et al.The haptenation theory of vitiligo and melanoma rejection:a close-up[J].Exp Dermatol,2011,20(4):376-382.
[16]Zhu MC,Liu CG,Wang DX,et al.Detection of serum anti-melanocyte antibodies and identification of related antigens in patients with vitiligo[J].Genet Mol Res,2015,(14):160-173.
[17]Bellei B,Pitisci A,Ottaviani M,et al.Vitiligo:A possible model of degenerative diseases[J].PLoS One,2013,(8):e59782.
[18]Qiu L,Song Z,Setaluri V.Oxidative stress and vitiligo:The Nrf2-AREsignaling connection[J].J Invest Dermatol,2014,(134):2074-2076.
[19]Kim JY,Lee EJ,Seo J,et al.Impact of HMGB1 on melanocytic survival and its involvement in the pathogenesis of vitiligo[J].BrJ Dermatol,2017,(176):1558-1568.
[20]Kumar R,Parsad D,Kanwar AJ,et al.Altered levels of LXR-a:Crucial implications in the pathogenesis of vitiligo[J].Exp Dermatol,2012,(21):853-858.
[21]Grimes PE,Sevall JS,Vodjani A.Cvtomegalovirus DNA identified in skin biopsy soecimens of patients with vitiligo[J].J Am Acad Dermatol,1992,15-284.
[22]AlGhamdi K,Kumar A,Moussa N.The role of vitamin D in melanogenesis with an emphasis on vitiligo[J].Indian J Dermatol Venereol Leprol,2013,79(6):750-758.
[23]杨励,王雷,孙林潮,等.维生素D受体基因多态性与白癜风的相关性研究[J].中国美容医学,2017,16(3):302-304.
[24]高天文,李强,李春英,等.白癜风2008例临床分析[J].中国皮肤性病学杂志,2002,16(5):304-306.
[25]周妙妮,许爱娥.白癜风与氧化抗氧化失衡[J].国际皮肤病学杂志,2007,33(5):281-283.
[26]乔树芳.曝晒对白癜风影响及对策研究进展[J].皮肤病与性病,2010,32(2):22-23.
[2]Alkhateeb A,Fain PR,Thody A,et al.Epidemiology of vitiligo and associated autoimmune diseases in Caucasian probands and theirfamilies[J].Pigment Cell Res,2003,(16):208-214.
[3]Spritz RA.The genetics of generalized vitiligo:Autoimmune pathways and an inverse relationship with malignant melanoma[J].Genome Med,2010,19(2):78.
[4]Wang P,Li Y,Nie H,et al.The changes of gene expression profiling between segmental vitiligo,generalized vitiligo and healthy individual[J].J Dermatol Sci,2016,(84):40-9.
[5]?ahmatova L,Tankov S,Prans E,et al.MicroRNA-155 is Dysregulated in the Skin of Patients withVitiligo and Inhibits Melanogenesis-associated Genes in Melanocytesand Keratinocytes[J].Acta Derm Venereol,2016,(96):742-747.
[6]Traks T,Keermann M,Karelson M,et al.Polymorphisms in Tolllike receptor genes are associated withvitiligo[J].Front Genet,2015,(6):278.
[7]Le Poole IC,van den Wijngaard RM,Westerhof W,et al.Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance[J].Am J Pathol,1996,(148):1219-1228.
[8]Allard EL,Hardy MP,Leignadier J,et al.Overexpression of IL-21promotes massive CD8+memory T cell accumulation[J].Eur J Immunol,2007,(37):3069-3077.
[9]Harris JE,Harris TH,Weninger W,et al.A mouse model of vitiligo with focused epidermal depigmentation requires IFN-g for autoreactive CD8+T-cell accumulation in the skin[J].J Invest Dermatol,2012,(132):1869-1876.
[10]李博为,李舒丽,杨钰琪,等.白癜风免疫微环境对黑素细胞CX-CL10表达的影响[J].中国麻风皮肤病杂志,2017,33(1):8-11.
[11]Singh RK,Lee KM,Vujkovic-Cvijin I,et al.The role of IL-17 in vitiligo:A review[J].Autoimmun Rev,2016,(15):397-404.
[12]Zhou L,Shi YL,Li K,et al.Increased circulating Th17 cells and elevated serum levels of TGF-beta and IL-21 are correlated with human non-segmental vitiligo development Pigment Cell Melanoma[J].Res,2015,(28):324-329.
[13]Bhardwaj S,Rani S,Srivastava N,et al.Increased systemic and epidermal levels of IL-17A and IL-1β promotes progression of non-segmental vitiligo[J].Cytokine,2017,(91):153-161.
[14]Naughton GK,Eisinger M,Bystryn JC.Antibodies to normal human melanocytes in vitiligo[J].J Exp Med,1983,158(1):246-251.
[15]Westerhof W,Manini P,Napolitano A,et al.The haptenation theory of vitiligo and melanoma rejection:a close-up[J].Exp Dermatol,2011,20(4):376-382.
[16]Zhu MC,Liu CG,Wang DX,et al.Detection of serum anti-melanocyte antibodies and identification of related antigens in patients with vitiligo[J].Genet Mol Res,2015,(14):160-173.
[17]Bellei B,Pitisci A,Ottaviani M,et al.Vitiligo:A possible model of degenerative diseases[J].PLoS One,2013,(8):e59782.
[18]Qiu L,Song Z,Setaluri V.Oxidative stress and vitiligo:The Nrf2-AREsignaling connection[J].J Invest Dermatol,2014,(134):2074-2076.
[19]Kim JY,Lee EJ,Seo J,et al.Impact of HMGB1 on melanocytic survival and its involvement in the pathogenesis of vitiligo[J].BrJ Dermatol,2017,(176):1558-1568.
[20]Kumar R,Parsad D,Kanwar AJ,et al.Altered levels of LXR-a:Crucial implications in the pathogenesis of vitiligo[J].Exp Dermatol,2012,(21):853-858.
[21]Grimes PE,Sevall JS,Vodjani A.Cvtomegalovirus DNA identified in skin biopsy soecimens of patients with vitiligo[J].J Am Acad Dermatol,1992,15-284.
[22]AlGhamdi K,Kumar A,Moussa N.The role of vitamin D in melanogenesis with an emphasis on vitiligo[J].Indian J Dermatol Venereol Leprol,2013,79(6):750-758.
[23]杨励,王雷,孙林潮,等.维生素D受体基因多态性与白癜风的相关性研究[J].中国美容医学,2017,16(3):302-304.
[24]高天文,李强,李春英,等.白癜风2008例临床分析[J].中国皮肤性病学杂志,2002,16(5):304-306.
[25]周妙妮,许爱娥.白癜风与氧化抗氧化失衡[J].国际皮肤病学杂志,2007,33(5):281-283.
[26]乔树芳.曝晒对白癜风影响及对策研究进展[J].皮肤病与性病,2010,32(2):22-23.