NB-UVB对银屑病患者外周血CC型趋化因子（MCP-1，MIP-1α）和CCR1mRNA的影响及意义
|
摘要
银屑病是一种慢性炎症性自身免疫性疾病,但其发病机制和治疗仍是世界难题。近几年银屑病与趋化因子及受体关系的研究成为热点。本次研究我们采用ELISA方法检测NB-UVB治疗寻常型银屑病患者前后外周血CC型趋化因子MCP-1及MIP-1α水平的变化,RT-PCR方法检测寻常型银屑病患者外周血单一核细胞CC型趋化因子受体CCR1mRNA的表达。以探讨NB-UVB是否可能通过影响患者外周血某些CC型趋化因子或受体的表达而达到治疗银屑病的目的。
目的:检测窄谱中波紫外线(NB-UVB)对银屑病患者外周血CC型趋化因子(MCP-1,MIP-1α)及CC型趋化因子受体1(CCR1)表达水平的影响。探讨NB-UVB是否通过影响银屑病患者外周血MCP-1和MIP-1α及CCR1的表达而发挥作用,为NB-UVB治疗银屑病提供更多的理论依据。
方法:采用双抗体酶联免疫吸附法(ELISA)分别检测NB-UVB照射治疗银屑病患者前后外周血CC型趋化因子MCP-1及MIP-1α的值。采用RT-PCR法检测NB-UVB照射治疗患者前后外周血单一核细胞CCR1mRNA表达水平。
结果:寻常型银屑病患者治疗前外周血中MCP-1及MIP-1α的值都明显高于正常对照组,照射治疗15次后,患者外周血中MCP-1较治疗前明显降低,差异具有统计学意义(P<0.01)。而MIP-1α与治疗前比较差异无统计学意义(P>0.05)。寻常型银屑病患者治疗前外周血单一核细胞CCR1mRNA表达明显高于正常对照组,照射治疗15次后,外周血单一核细胞CCR1mRNA表达较治疗前明显降低,差异具有统计学意义(P<0.01)。
结论:NB-UVB可能通过降低银屑病患者外周血MCP-1及CCR1的表达而发挥作用。
Psoriasis is a chronic inflammatory autoimmune disease. However, the pathogenesis and treatment remains the world's problems. In recent years, the relationship between psoriasis and chemokines (include chemokine receptors) has become popular. In this study, enzyme-linked immunosorbent assay (ELISA) technique was used to detect CC chemokines MCP-1 and MIP-1αvalues in peripheral blood of psoriasis patients before treatment and patients after NB-UVB treatment and healthy controls; Reverse transcription-polymerase chain reaction (RT-PCR) technique was applied to semi-quantitatively analyze CCR1 mRNA expression levels in peripheral blood mononuclear cells (PBMC). In order to investigate whether NB-UVB through regulate the expression of certain CC-type chemokine (or its receptor) to achieve the purpose of anti-psoriasis.
Objective: To observe effect of narrow-band ultraviolet B (NB-UVB) phototherapy on peripheral blood CC chemokines (MCP-1, MIP-1α) and CC chemokine receptor 1 (CCR1) in patients with psoriasis. Further clarify whether NB-UVB through influencing the expression of MCP-1 and MIP-1αand CCR1 to achieve the purposes of therapy, provide more theoretical basis for NB-UVB in the treatment of psoriasis.
Methods: Serum levels of MCP-1 and MIP-1αwere measured by double-antibody enzyme-linked immunosorbent assay (ELISA) in patients with psoriasis vulgaris before and after the treatment with NB-UVB. CCR1mRNA expression levels in peripheral blood were detected by RT-PCR.
Results: Before treatment, MCP-1 and MIP-1αvalues in peripheral blood of patients with psoriasis vulgaris were significantly higher than the normal controls. After 15 times phototherapy, the serum levels of MCP-1 decreased significantly, the difference has statistically significant (P <0.01). While the serum levels of MIP-1αshowed no significant difference before the treatment than after the treatment (P> 0.05). CCR1 levels in peripheral blood mononuclear cells of psoriasis patients before treatment was significantly higher than those in the normal controls. After 15 times phototherapy, CCR1 expression levels in peripheral blood mononuclear cells decreased significantly, the difference has statistically significant (P <0.01).
Conclusion: NB-UVB partly through reducing the expression of MCP-1 and CCR1 in peripheral blood of psoriasis to achieve treatment objectives.
目的:检测窄谱中波紫外线(NB-UVB)对银屑病患者外周血CC型趋化因子(MCP-1,MIP-1α)及CC型趋化因子受体1(CCR1)表达水平的影响。探讨NB-UVB是否通过影响银屑病患者外周血MCP-1和MIP-1α及CCR1的表达而发挥作用,为NB-UVB治疗银屑病提供更多的理论依据。
方法:采用双抗体酶联免疫吸附法(ELISA)分别检测NB-UVB照射治疗银屑病患者前后外周血CC型趋化因子MCP-1及MIP-1α的值。采用RT-PCR法检测NB-UVB照射治疗患者前后外周血单一核细胞CCR1mRNA表达水平。
结果:寻常型银屑病患者治疗前外周血中MCP-1及MIP-1α的值都明显高于正常对照组,照射治疗15次后,患者外周血中MCP-1较治疗前明显降低,差异具有统计学意义(P<0.01)。而MIP-1α与治疗前比较差异无统计学意义(P>0.05)。寻常型银屑病患者治疗前外周血单一核细胞CCR1mRNA表达明显高于正常对照组,照射治疗15次后,外周血单一核细胞CCR1mRNA表达较治疗前明显降低,差异具有统计学意义(P<0.01)。
结论:NB-UVB可能通过降低银屑病患者外周血MCP-1及CCR1的表达而发挥作用。
Psoriasis is a chronic inflammatory autoimmune disease. However, the pathogenesis and treatment remains the world's problems. In recent years, the relationship between psoriasis and chemokines (include chemokine receptors) has become popular. In this study, enzyme-linked immunosorbent assay (ELISA) technique was used to detect CC chemokines MCP-1 and MIP-1αvalues in peripheral blood of psoriasis patients before treatment and patients after NB-UVB treatment and healthy controls; Reverse transcription-polymerase chain reaction (RT-PCR) technique was applied to semi-quantitatively analyze CCR1 mRNA expression levels in peripheral blood mononuclear cells (PBMC). In order to investigate whether NB-UVB through regulate the expression of certain CC-type chemokine (or its receptor) to achieve the purpose of anti-psoriasis.
Objective: To observe effect of narrow-band ultraviolet B (NB-UVB) phototherapy on peripheral blood CC chemokines (MCP-1, MIP-1α) and CC chemokine receptor 1 (CCR1) in patients with psoriasis. Further clarify whether NB-UVB through influencing the expression of MCP-1 and MIP-1αand CCR1 to achieve the purposes of therapy, provide more theoretical basis for NB-UVB in the treatment of psoriasis.
Methods: Serum levels of MCP-1 and MIP-1αwere measured by double-antibody enzyme-linked immunosorbent assay (ELISA) in patients with psoriasis vulgaris before and after the treatment with NB-UVB. CCR1mRNA expression levels in peripheral blood were detected by RT-PCR.
Results: Before treatment, MCP-1 and MIP-1αvalues in peripheral blood of patients with psoriasis vulgaris were significantly higher than the normal controls. After 15 times phototherapy, the serum levels of MCP-1 decreased significantly, the difference has statistically significant (P <0.01). While the serum levels of MIP-1αshowed no significant difference before the treatment than after the treatment (P> 0.05). CCR1 levels in peripheral blood mononuclear cells of psoriasis patients before treatment was significantly higher than those in the normal controls. After 15 times phototherapy, CCR1 expression levels in peripheral blood mononuclear cells decreased significantly, the difference has statistically significant (P <0.01).
Conclusion: NB-UVB partly through reducing the expression of MCP-1 and CCR1 in peripheral blood of psoriasis to achieve treatment objectives.
引文
[1]ROUSSAKI-SCHULZE AV,KOUSKOUKIS C,PETINAKI E,et al.Evaluation of cytokine serum levels in Patients with Plaque-tyPe Psoriasis[J].Int J Clin Pharmacol Res,2005,25(4):169-173.
[2]BONIFACE K,LECRON JC,BERNARD FX,et al.Keratinocytes as targets for interleukin-10-related cytokines;A Putative role in the Pathogenesis of Psoriasis[J].Eur Cytokine New,2005,16(4);309-319.
[3]Springer TA. Traffic signals for lymphocyte recirculation and leuko cyte emigration: the multistep paradigm[ J ]. Cell, 1994, 76 (2) : 301 - 314.
[4]GASPARI AA.Innate and adaptive immunity and the PathoPhysiology of Psoriasis[J].J Am Acad Dermatol,2006,54(3):67-80.
[5]Christophers E. The immunopathology of psoriasis. Int Arch Allergy Immunol 1996;110:199-206.
[6]Schulz BS et al . J Immunol , 1993 ;151(8) :4399-4406
[7]Hatano Y, Katagiri K, Takayasu S. Increased levels in vivo of mR N A sfor IL28 and macrophage inflammatory protein21 alpha (MIP-1 alpha) , but not of RANTES mRNA in peripheral blood mononuclear cells of patients with atopic dermatitis (AD) . Clin Exp Immunol , 1999 ,117 (2) :2372243.
[8] Macchioni P , Boiardi L , Meliconi R , et al . Serum chemokines in patients with psoriatic arthritis treated with cyclosporin A. J Rheumatol , 1998 ,25 (2) :3202325.
[9] SIBA P. RAYCHAUDHURI1,WEN-YUE JIANG1, EUGENE M. FARBER1etal. Upregulation of RANTES in Psoriatic Keratinocytes: a Possible Pathogenic Mechanism for Psoriasis Acta Derm Venereol (Stockh) 1999; 79: 9-11
[10]唐玲,于益芝,唐跃琼等。RANTES在银屑病患者外周血中的表达及其临床意义。China J Lepr Skin Dis. [J] 2003 ,19 (1),28
[11]Bos JD, de Rie MA. The pathogenesis of psoriasis:immunological facts and speculations. Immunol Today1999; 20: 40– 46.
[12]Reinhard Gillitzer,Klaus Woff,Dan Tong etal.MCP-1mRNA Expression in Basal Keratinocytes of Psoriasis Lesion. J Invest Dermatol 1993(101):127-131
[13]唐玲,于益芝,陈洁等。他克莫司影响朗格汉斯细胞迁移机制的研究。中华皮肤科杂志。2004,37(11)
[14]唐玲,于益芝,陈洁等。维生素D3抑制角质形成细胞MCP21的表达。中国皮肤性病学杂志。2004,18(6)
[15] Conrad SM, Strauss-Ayali D, Field AE, et al. Leishmania-derived murine monocyte chemoattractant protein 1 enhances the recruitment of a restrictive population of CC chemokine receptor 2-positive macrophages. Infect Immun 2007;75:653-65
[1] . Sch(?)n MP, and Ruzicka T. Psoriasis: the plot thickens.Nat Immunol 2001; 2: 91.
[2]. Nickoloff BJ, Mitra RS, Varani J, Dixit VM, Polverini PJ. Aberrant production of interleukin-8 and thrombospondin-1 by psoriatic keratinocytes mediates angiogenesis. Am J Pathol 1994; 144: 820-8.
[3]Vanbervliet B, Homey B, Durand I, Massacrier C, Ait-Yahia S, de Bouteiller O, Vicari A, Caux C. Sequential involvement of CCR2 and CCR6 ligands for immature dendritic cell recruitment: possible role at inflamed epithelial surfaces. Eur J Immunol 2002; 32: 231-42.
[4] Homey B, D ieu2No sjean M C, W iesenbo rn A , et al. Up-regulation of macrophage inflammato ry p ro tein-3alpha(?) CCL 20 and CC chemok ine recep to r 6 in p so riasis[J ]. J Immuno l, 2000, 164 (12) : 6621- 6632.
[5]唐玲,李泉,陈洁等RANTES在银屑病患者角质形成细胞中的表达及其作用,中国麻风皮肤病杂志,2003,19(5):426-427
[6] GoebelerM , Tok soyA , Spandau U , et al. The C-X-C chemok ine M ig is h igh ly exp ressed in the pap illae of p so riatic lesions [J ]. J Patho l, 1998, 184 (1) : 89- 95
[7]Raychaudhuri S P, J iangW Y, Farber E M. Cellular localization of fractalk ine at sites of inflammation: antigen-presenting cells in psoriasis express high levels of fractalk ine [J ]. Br J Dermato l, 2001, 144 (6) : 1105-1113.
[8]刘文韬,朱里,胡志国,等.Fractalkine和其受体Cx3CR1在寻常性银屑病中的表达及意义.中国皮肤性病学杂志2007,21(4):193-195
[9]Van Coillie E, Van Damme J, Opdenakker G. The MCP/eotaxin subfamily of CC chemokines. Cytokine Growth Factor Rev. 1999 10:61–86
[10] Palframan RT, Jung S, Cheng G, Weninger W, Luo Y, Dorf M, Littman DR, Rollins BJ, Zweerink H, Rot A, von Andrian UH. Inflammatory chemokine transport and presentation in HEV: a remote control mechanism for monocyte recruitment to lymph nodes in inflamed tissues. J Exp Med. 2001;194:1361–1373
[11] Nakamura K, Williams IR , Kupper TS. Keratinocyte-derived monocyte chemoattractant protein 1 (MCP-1 ) : analysis in a transgenic model demonstrates MCP-1 can recruit dendritic and Langerhans cells to skin. J Invest Dermatol , 1995 ,105 (5) :635-643.
[12] Ross EL , D’Cruz D , Morrow WJ . Localized monocyte chemotactic pro tein-1 production correlates with T cell infiltration of synovium in patients with psoriatic arthritis. J Rheumatol , 2000 ,27 (10) :2432-2443.
[13]陈积愫,郑敏。寻常型银屑病患者血管内皮生长因子及单核细胞趋化因子-1表达的研究[J]。中华皮肤科杂志,2002,35(2):111-113
[14]唐玲,于益芝,李泉,等.寻常性银屑病血清MCP21的检测[J].中国皮肤性病学杂志, 2003, 17 (2) : 87 - 90.
[15]Yamazaki S,Yokozeki H,Satoh T,et a1.TNF-alpha,RANTES and MCP-1 are major chemoattractant of murine Langerhans cells to the regional lymph nodes[J].Exp Dermatol,1998,(1):35·41.
[16]俞星飞,劳力民,严建良等。寻常型银屑病患者血清单核细胞趋化因子-1、巨噬细胞炎性蛋白-1a和巨噬细胞衍生的趋化因子水平测定[J]。中华皮肤科杂志,2006,39(3):165-166
[17]贾玲芝,任万明,高军.寻常性银屑病患者血清MCP-1和MIP-3α的检测及意义[J].中国皮肤性病学杂志,2008,22(3):138-139
[18] Pohl D, Andrys C, BorskáLCC and CXC chemokines patterns in psoriasis determined by protein array method were influenced by Goeckerman's therapy. Acta Medica 2009;52(1):9-13
[19] Dieu-Nosjean MC , Massacrier C , Homey B , et al .Macrophage inflammatory protein 3alpha is expressed at inflamed epithelial surfaces and is the most potent chemokine known in attracting Langerhans cell precursors. J Exp Med , 2000 ,192 (5) :705-718.
[20] Lee SC, BurmmentME, Shaha buddin S, et al. Cutaneous injection of human subjectswithmacrophage inflammatory p rotein-l alpha induces significant recruitment of neutrophi1 s and monocytes [ J ]. J Imm unol, 2000,161 (6) : 3 392-401.
[21]何焱玲,丁桂凤,朱铁君神经肽CGRP对银屑病单核细胞趋化功能的调节临床皮肤科杂志2002:31(7)407-409
[22] Goebeler M, Toksoy A, Spandau Uetal. 1998 Jan;184(1):89-95
[23] Hatano Y, Katagiri K, Takayasu S. Increased levels in vivo of mRNAs for IL-8 and macrophage inflammatory protein-1α( MIP-1α) , but not of RANTES mRNA in peripheral blood mononuclear cells of patients with atopic dermatitis ( AD) . Clin Exp Immunol, 1999, 117: 237-243
[24] Gao, J.L.; Kuhns, D.B.; Tiffany, H.L.etal,Structure and functional expression of the human macrophage inflammatory protein 1 alpha/RANTES receptor.J. Exp. Med. 1993, 177(5), 1421-7.
[25] Neote, K.; DiGregorio, D.; Mak, J.Y.;etal, Molecular cloning, functional expression, and signaling characteristics of a C-C chemokine receptor. .J Cell 1993;72(3):415-25
[26] Murdoch C and Finn A. Chemokine receptors and their role in inflammation and infectious diseases.Blood,2000,95(10):3032-3043
[27] Barnes, D.A.; Tse, J.; Kaufhold, M.; etal. Polyclonal antibody directed against human RANTES ameliorates disease in the Lewis rat adjuvant-induced arthritis model. .J. Clin. Invest. 1998, 101(12),2910-9.
[28] Pattison, J.; Nelson, P.J.; Huie, P.etal. RANTES chemokine expression in cell-mediated transplant rejection of the kidney.Lancet1994: 343(8891):209-11
[29] Pattison, J.; Nelson, P.J.; Huie, P.; von Leuttichau, I.; Farshid, G.; Sibley, R.K.; Krensky, A.M. Lancet 1996,15, 1194.
[30] Raychaudhuri SP,jiang WY,Farber EM,etal.Upregulation of RANTES in psoriatic keratinocrtes: a possible pathogenic mechanism for psoriasis.Acta Derm Veneral,1999,79(1):9-11.
[31]唐玲,于益芝,唐跃琼等。RANTES在银屑病患者外周血中的表达及其临床意义。China J Lepr Skin Dis.[J] 2003 :19 (1)
[32]杨桂兰,陈志强,郑家润等。寻常性银屑病患者外周血中性粒细胞中趋化因子受体的表达。临床皮肤科杂志2006:35(2)
[1] Tjioe M, Smits T, van de Kerkhof PC, et al. The differential effect of broad band vs narrow band UVB with respect to photodamage and cutaneous inflammation[J]. Exp Dermatol, 2003, 12 (6): 729- 733
[2] Kircik L, Bagel J, Korman N, Menter A, Elmets CA, Koo J, Yang YC, Chiou CF, Dann F, Stevens SR; Unite Study Group. Utilization of narrow-band ultraviolet light B therapy and etanercept for the treatment of psoriasis (UNITE): efficacy, safety, and patient-reported outcomes. [J] Drugs Dermatol. 2008 Mar;7(3):245-53
[3]苗青,王丽,李红文。阿维A联合窄谱中波紫外线照射治疗寻常型银屑病临床疗效分析[J]中国皮肤性病学杂志2007 03, 21(3)160-161
[4]Ibbotson SH,Bilsland D,Cox NH,etal.An update and guidance on narrowband ultraviolet B phototherapy: a British Photodermatology Group Workshop Report.Br J Dermatol,2004,151(2):283-297.
[5] Yones SS,Palmer RA,Garibaldinos TT,etal.Randomized double-blind trial of the treatment of chronic plaque psoriasis:erricacy of psoralen-UV-A therapy vs narrowband UV-B therapy Arch Dermatol,2006,142(7):836-842
[6]杨海珍,汪科,段周英等,窄谱UVB治疗寻常性银屑病的临床研究,中国皮肤性病学杂志2005,19(3):151-153
[7]樊昕,王刚,刘玉峰UVB照射前后银屑病T细胞趋化因子受体7及其基因的表达。[J]细胞与分子免疫学杂志2006, 22 (4):490-492
[8]冯同喜,曹晶晶,杜华等。窄谱中波紫外线治疗对银屑病患者趋化因子受体CCR1 mRNA表达的影响。[J]第四军医大学学报. 2008, 29 (21):1994-1996。
[9]冯同喜,曹晶晶,杜华等.窄谱中波紫外线治疗对银屑病患者CCR2 mRNA表达的影响.[J]中国皮肤性病学杂志。2008,22(9):532-534.
[10] Kondo S, Yoneta A, Yazawa H, etal. Downregulation of CXCR-2 but not CXCR-1 expression by human keratinocytes by UVB.[J] Cell Physiol. 2000 Mar;182(3):366-70
[11] Piskin G, Sylva- Steenland RM, Bos JD, et al. T cells in psoriatic lesional skin that survive conventional therapy with NB- UVB radiation display reduced IFN-gamma expression[J]. Arch Dermatol Res, 2004, 295(12): 509- 516
[12]Waters IB,OzawaM, Cardinale, etal. Narrow band (312nm) UVB suppresses Iaterferon r and Iaterleukin ( IL) -2 and increases IL-4 Transcirpes[ J ]. Arch Dermatol, 2003, 139: 155 - 161.
[13] Serwin AB, Sokolowska M, Chodynicka B. Soluble Tuble tumor necrosis factor alpha receptor type 1 in psoriasis patients treated with narrowband ultraviolet B.photodermatol Photoimmunol Photomed.2005.21(4):210-211
[14]el-Ghorr AA,Norval, Lappin MB, etal. The effect of chrinic low-dose UVB radiation on langerhans cells,sunburn cells, urocanic acid isomers, contact hypersensitivity and serum immunoglobulins in mice.Photochem Photobiol,1995,62(2):326-332
[15] Hamakawa M, Sugihara A. Ultraviolet B radiation suppresses Langerhans cell migration in the dermis by down - regulation of al2 pha4 integrin. Photodermatol Photoimmunol Photomed 2006 ;22(3) : 116– 123
[16] Szepietowski JC , Morita A , Tsuji T. Ultraviolet B induces mast cell apoptosis : a hypothetical mechanismof ultraviolet B treatment for uraemic pru2 ritus[J ]1 Med Hypotheses , 2002 , 58(2) : 167～1701
[17] Aufiero BM, Talwar H , Young C , etal. Narrow - band UVB induces apoptosis in human keratinocytes. J Photochem Photobiol B2006 ;82 :132– 139
[18]Ozawa M, Ferenczi K, Kikuchi T, Cardinale I, Austin LM, Coven TR, et al. 312-nanometer ultraviolet B light (narrow-band UVB) induces apoptosis of T cells within psoriatic lesions. J Exp Med 1999; 189: 711–718. [19 ] Hansson A,BloorBK, Sarang Z, et al. Analysis of p roliferation, apoptosis and keratin exp ression in cultured normal and immortalized human buccal keratinocytes [ J ]. Eur J Oral Sci, 2003, 111 (1) , 34 - 41.
[20] Walter IB,Burack LH, Coven TR,etal. Suberythemogenic narrow-band UVB is markedly more effective than conventional UVB in treatment of psoriasis vulgaris,J Am Acad Dermatol,1999,40(6 pt 1): 893-900
[21]Lehmann B, Knuschke P, Meurer M. Effect of UVB radiation emitted from the narrowband TL- 01 lamp (311 nm) on the calcitriol synthesis in organotypic culturesof keratinocytes [J]. Exp Dermatol, 2005, 14(2): 153
[22] Aufiero BM, Talwar H, Young C,etal. Narrow - band UVB induces apoptosis in human keratinocytes[J ] . Photochenistry and photo-Biology B , 2006 , 82 :132～139
[23]于波,钟绮丽,张杰等。NB-UVB治疗银屑病的疗效及其对皮损角质形成细胞周期蛋白D1和E的影响[J]中国麻风皮肤病杂志2007 ,08 23(8):649-651
[2]BONIFACE K,LECRON JC,BERNARD FX,et al.Keratinocytes as targets for interleukin-10-related cytokines;A Putative role in the Pathogenesis of Psoriasis[J].Eur Cytokine New,2005,16(4);309-319.
[3]Springer TA. Traffic signals for lymphocyte recirculation and leuko cyte emigration: the multistep paradigm[ J ]. Cell, 1994, 76 (2) : 301 - 314.
[4]GASPARI AA.Innate and adaptive immunity and the PathoPhysiology of Psoriasis[J].J Am Acad Dermatol,2006,54(3):67-80.
[5]Christophers E. The immunopathology of psoriasis. Int Arch Allergy Immunol 1996;110:199-206.
[6]Schulz BS et al . J Immunol , 1993 ;151(8) :4399-4406
[7]Hatano Y, Katagiri K, Takayasu S. Increased levels in vivo of mR N A sfor IL28 and macrophage inflammatory protein21 alpha (MIP-1 alpha) , but not of RANTES mRNA in peripheral blood mononuclear cells of patients with atopic dermatitis (AD) . Clin Exp Immunol , 1999 ,117 (2) :2372243.
[8] Macchioni P , Boiardi L , Meliconi R , et al . Serum chemokines in patients with psoriatic arthritis treated with cyclosporin A. J Rheumatol , 1998 ,25 (2) :3202325.
[9] SIBA P. RAYCHAUDHURI1,WEN-YUE JIANG1, EUGENE M. FARBER1etal. Upregulation of RANTES in Psoriatic Keratinocytes: a Possible Pathogenic Mechanism for Psoriasis Acta Derm Venereol (Stockh) 1999; 79: 9-11
[10]唐玲,于益芝,唐跃琼等。RANTES在银屑病患者外周血中的表达及其临床意义。China J Lepr Skin Dis. [J] 2003 ,19 (1),28
[11]Bos JD, de Rie MA. The pathogenesis of psoriasis:immunological facts and speculations. Immunol Today1999; 20: 40– 46.
[12]Reinhard Gillitzer,Klaus Woff,Dan Tong etal.MCP-1mRNA Expression in Basal Keratinocytes of Psoriasis Lesion. J Invest Dermatol 1993(101):127-131
[13]唐玲,于益芝,陈洁等。他克莫司影响朗格汉斯细胞迁移机制的研究。中华皮肤科杂志。2004,37(11)
[14]唐玲,于益芝,陈洁等。维生素D3抑制角质形成细胞MCP21的表达。中国皮肤性病学杂志。2004,18(6)
[15] Conrad SM, Strauss-Ayali D, Field AE, et al. Leishmania-derived murine monocyte chemoattractant protein 1 enhances the recruitment of a restrictive population of CC chemokine receptor 2-positive macrophages. Infect Immun 2007;75:653-65
[1] . Sch(?)n MP, and Ruzicka T. Psoriasis: the plot thickens.Nat Immunol 2001; 2: 91.
[2]. Nickoloff BJ, Mitra RS, Varani J, Dixit VM, Polverini PJ. Aberrant production of interleukin-8 and thrombospondin-1 by psoriatic keratinocytes mediates angiogenesis. Am J Pathol 1994; 144: 820-8.
[3]Vanbervliet B, Homey B, Durand I, Massacrier C, Ait-Yahia S, de Bouteiller O, Vicari A, Caux C. Sequential involvement of CCR2 and CCR6 ligands for immature dendritic cell recruitment: possible role at inflamed epithelial surfaces. Eur J Immunol 2002; 32: 231-42.
[4] Homey B, D ieu2No sjean M C, W iesenbo rn A , et al. Up-regulation of macrophage inflammato ry p ro tein-3alpha(?) CCL 20 and CC chemok ine recep to r 6 in p so riasis[J ]. J Immuno l, 2000, 164 (12) : 6621- 6632.
[5]唐玲,李泉,陈洁等RANTES在银屑病患者角质形成细胞中的表达及其作用,中国麻风皮肤病杂志,2003,19(5):426-427
[6] GoebelerM , Tok soyA , Spandau U , et al. The C-X-C chemok ine M ig is h igh ly exp ressed in the pap illae of p so riatic lesions [J ]. J Patho l, 1998, 184 (1) : 89- 95
[7]Raychaudhuri S P, J iangW Y, Farber E M. Cellular localization of fractalk ine at sites of inflammation: antigen-presenting cells in psoriasis express high levels of fractalk ine [J ]. Br J Dermato l, 2001, 144 (6) : 1105-1113.
[8]刘文韬,朱里,胡志国,等.Fractalkine和其受体Cx3CR1在寻常性银屑病中的表达及意义.中国皮肤性病学杂志2007,21(4):193-195
[9]Van Coillie E, Van Damme J, Opdenakker G. The MCP/eotaxin subfamily of CC chemokines. Cytokine Growth Factor Rev. 1999 10:61–86
[10] Palframan RT, Jung S, Cheng G, Weninger W, Luo Y, Dorf M, Littman DR, Rollins BJ, Zweerink H, Rot A, von Andrian UH. Inflammatory chemokine transport and presentation in HEV: a remote control mechanism for monocyte recruitment to lymph nodes in inflamed tissues. J Exp Med. 2001;194:1361–1373
[11] Nakamura K, Williams IR , Kupper TS. Keratinocyte-derived monocyte chemoattractant protein 1 (MCP-1 ) : analysis in a transgenic model demonstrates MCP-1 can recruit dendritic and Langerhans cells to skin. J Invest Dermatol , 1995 ,105 (5) :635-643.
[12] Ross EL , D’Cruz D , Morrow WJ . Localized monocyte chemotactic pro tein-1 production correlates with T cell infiltration of synovium in patients with psoriatic arthritis. J Rheumatol , 2000 ,27 (10) :2432-2443.
[13]陈积愫,郑敏。寻常型银屑病患者血管内皮生长因子及单核细胞趋化因子-1表达的研究[J]。中华皮肤科杂志,2002,35(2):111-113
[14]唐玲,于益芝,李泉,等.寻常性银屑病血清MCP21的检测[J].中国皮肤性病学杂志, 2003, 17 (2) : 87 - 90.
[15]Yamazaki S,Yokozeki H,Satoh T,et a1.TNF-alpha,RANTES and MCP-1 are major chemoattractant of murine Langerhans cells to the regional lymph nodes[J].Exp Dermatol,1998,(1):35·41.
[16]俞星飞,劳力民,严建良等。寻常型银屑病患者血清单核细胞趋化因子-1、巨噬细胞炎性蛋白-1a和巨噬细胞衍生的趋化因子水平测定[J]。中华皮肤科杂志,2006,39(3):165-166
[17]贾玲芝,任万明,高军.寻常性银屑病患者血清MCP-1和MIP-3α的检测及意义[J].中国皮肤性病学杂志,2008,22(3):138-139
[18] Pohl D, Andrys C, BorskáLCC and CXC chemokines patterns in psoriasis determined by protein array method were influenced by Goeckerman's therapy. Acta Medica 2009;52(1):9-13
[19] Dieu-Nosjean MC , Massacrier C , Homey B , et al .Macrophage inflammatory protein 3alpha is expressed at inflamed epithelial surfaces and is the most potent chemokine known in attracting Langerhans cell precursors. J Exp Med , 2000 ,192 (5) :705-718.
[20] Lee SC, BurmmentME, Shaha buddin S, et al. Cutaneous injection of human subjectswithmacrophage inflammatory p rotein-l alpha induces significant recruitment of neutrophi1 s and monocytes [ J ]. J Imm unol, 2000,161 (6) : 3 392-401.
[21]何焱玲,丁桂凤,朱铁君神经肽CGRP对银屑病单核细胞趋化功能的调节临床皮肤科杂志2002:31(7)407-409
[22] Goebeler M, Toksoy A, Spandau Uetal. 1998 Jan;184(1):89-95
[23] Hatano Y, Katagiri K, Takayasu S. Increased levels in vivo of mRNAs for IL-8 and macrophage inflammatory protein-1α( MIP-1α) , but not of RANTES mRNA in peripheral blood mononuclear cells of patients with atopic dermatitis ( AD) . Clin Exp Immunol, 1999, 117: 237-243
[24] Gao, J.L.; Kuhns, D.B.; Tiffany, H.L.etal,Structure and functional expression of the human macrophage inflammatory protein 1 alpha/RANTES receptor.J. Exp. Med. 1993, 177(5), 1421-7.
[25] Neote, K.; DiGregorio, D.; Mak, J.Y.;etal, Molecular cloning, functional expression, and signaling characteristics of a C-C chemokine receptor. .J Cell 1993;72(3):415-25
[26] Murdoch C and Finn A. Chemokine receptors and their role in inflammation and infectious diseases.Blood,2000,95(10):3032-3043
[27] Barnes, D.A.; Tse, J.; Kaufhold, M.; etal. Polyclonal antibody directed against human RANTES ameliorates disease in the Lewis rat adjuvant-induced arthritis model. .J. Clin. Invest. 1998, 101(12),2910-9.
[28] Pattison, J.; Nelson, P.J.; Huie, P.etal. RANTES chemokine expression in cell-mediated transplant rejection of the kidney.Lancet1994: 343(8891):209-11
[29] Pattison, J.; Nelson, P.J.; Huie, P.; von Leuttichau, I.; Farshid, G.; Sibley, R.K.; Krensky, A.M. Lancet 1996,15, 1194.
[30] Raychaudhuri SP,jiang WY,Farber EM,etal.Upregulation of RANTES in psoriatic keratinocrtes: a possible pathogenic mechanism for psoriasis.Acta Derm Veneral,1999,79(1):9-11.
[31]唐玲,于益芝,唐跃琼等。RANTES在银屑病患者外周血中的表达及其临床意义。China J Lepr Skin Dis.[J] 2003 :19 (1)
[32]杨桂兰,陈志强,郑家润等。寻常性银屑病患者外周血中性粒细胞中趋化因子受体的表达。临床皮肤科杂志2006:35(2)
[1] Tjioe M, Smits T, van de Kerkhof PC, et al. The differential effect of broad band vs narrow band UVB with respect to photodamage and cutaneous inflammation[J]. Exp Dermatol, 2003, 12 (6): 729- 733
[2] Kircik L, Bagel J, Korman N, Menter A, Elmets CA, Koo J, Yang YC, Chiou CF, Dann F, Stevens SR; Unite Study Group. Utilization of narrow-band ultraviolet light B therapy and etanercept for the treatment of psoriasis (UNITE): efficacy, safety, and patient-reported outcomes. [J] Drugs Dermatol. 2008 Mar;7(3):245-53
[3]苗青,王丽,李红文。阿维A联合窄谱中波紫外线照射治疗寻常型银屑病临床疗效分析[J]中国皮肤性病学杂志2007 03, 21(3)160-161
[4]Ibbotson SH,Bilsland D,Cox NH,etal.An update and guidance on narrowband ultraviolet B phototherapy: a British Photodermatology Group Workshop Report.Br J Dermatol,2004,151(2):283-297.
[5] Yones SS,Palmer RA,Garibaldinos TT,etal.Randomized double-blind trial of the treatment of chronic plaque psoriasis:erricacy of psoralen-UV-A therapy vs narrowband UV-B therapy Arch Dermatol,2006,142(7):836-842
[6]杨海珍,汪科,段周英等,窄谱UVB治疗寻常性银屑病的临床研究,中国皮肤性病学杂志2005,19(3):151-153
[7]樊昕,王刚,刘玉峰UVB照射前后银屑病T细胞趋化因子受体7及其基因的表达。[J]细胞与分子免疫学杂志2006, 22 (4):490-492
[8]冯同喜,曹晶晶,杜华等。窄谱中波紫外线治疗对银屑病患者趋化因子受体CCR1 mRNA表达的影响。[J]第四军医大学学报. 2008, 29 (21):1994-1996。
[9]冯同喜,曹晶晶,杜华等.窄谱中波紫外线治疗对银屑病患者CCR2 mRNA表达的影响.[J]中国皮肤性病学杂志。2008,22(9):532-534.
[10] Kondo S, Yoneta A, Yazawa H, etal. Downregulation of CXCR-2 but not CXCR-1 expression by human keratinocytes by UVB.[J] Cell Physiol. 2000 Mar;182(3):366-70
[11] Piskin G, Sylva- Steenland RM, Bos JD, et al. T cells in psoriatic lesional skin that survive conventional therapy with NB- UVB radiation display reduced IFN-gamma expression[J]. Arch Dermatol Res, 2004, 295(12): 509- 516
[12]Waters IB,OzawaM, Cardinale, etal. Narrow band (312nm) UVB suppresses Iaterferon r and Iaterleukin ( IL) -2 and increases IL-4 Transcirpes[ J ]. Arch Dermatol, 2003, 139: 155 - 161.
[13] Serwin AB, Sokolowska M, Chodynicka B. Soluble Tuble tumor necrosis factor alpha receptor type 1 in psoriasis patients treated with narrowband ultraviolet B.photodermatol Photoimmunol Photomed.2005.21(4):210-211
[14]el-Ghorr AA,Norval, Lappin MB, etal. The effect of chrinic low-dose UVB radiation on langerhans cells,sunburn cells, urocanic acid isomers, contact hypersensitivity and serum immunoglobulins in mice.Photochem Photobiol,1995,62(2):326-332
[15] Hamakawa M, Sugihara A. Ultraviolet B radiation suppresses Langerhans cell migration in the dermis by down - regulation of al2 pha4 integrin. Photodermatol Photoimmunol Photomed 2006 ;22(3) : 116– 123
[16] Szepietowski JC , Morita A , Tsuji T. Ultraviolet B induces mast cell apoptosis : a hypothetical mechanismof ultraviolet B treatment for uraemic pru2 ritus[J ]1 Med Hypotheses , 2002 , 58(2) : 167～1701
[17] Aufiero BM, Talwar H , Young C , etal. Narrow - band UVB induces apoptosis in human keratinocytes. J Photochem Photobiol B2006 ;82 :132– 139
[18]Ozawa M, Ferenczi K, Kikuchi T, Cardinale I, Austin LM, Coven TR, et al. 312-nanometer ultraviolet B light (narrow-band UVB) induces apoptosis of T cells within psoriatic lesions. J Exp Med 1999; 189: 711–718. [19 ] Hansson A,BloorBK, Sarang Z, et al. Analysis of p roliferation, apoptosis and keratin exp ression in cultured normal and immortalized human buccal keratinocytes [ J ]. Eur J Oral Sci, 2003, 111 (1) , 34 - 41.
[20] Walter IB,Burack LH, Coven TR,etal. Suberythemogenic narrow-band UVB is markedly more effective than conventional UVB in treatment of psoriasis vulgaris,J Am Acad Dermatol,1999,40(6 pt 1): 893-900
[21]Lehmann B, Knuschke P, Meurer M. Effect of UVB radiation emitted from the narrowband TL- 01 lamp (311 nm) on the calcitriol synthesis in organotypic culturesof keratinocytes [J]. Exp Dermatol, 2005, 14(2): 153
[22] Aufiero BM, Talwar H, Young C,etal. Narrow - band UVB induces apoptosis in human keratinocytes[J ] . Photochenistry and photo-Biology B , 2006 , 82 :132～139
[23]于波,钟绮丽,张杰等。NB-UVB治疗银屑病的疗效及其对皮损角质形成细胞周期蛋白D1和E的影响[J]中国麻风皮肤病杂志2007 ,08 23(8):649-651