Bianchi B, Campolmi P, Mavilia L, Danesi A, Rossi R, Cappugi P
Department of Dermatological Sciences, University of Florence, Via degli Alfani, 37, 50121 Florence, Italy.
J Eur Acad Dermatol Venereol. 2003 Jul;17(4):408-13. doi: 10.1046/j.1468-3083.2003.00758.x.
Various types of UVB radiation source (290-320 nm) are used in treating psoriasis and their therapeutic mechanism has been attributed to immunosuppressive properties. Recently, a new UVB source generated by a 308-nm excimer laser has been introduced for the treatment of psoriasis.
In this study we investigated the immunohistochemical evaluation of T cells and the expression of various apoptosis-related molecules in the psoriatic hyperproliferative skin before and after treatment with 308-nm monochromatic excimer light (MEL).
Ten patients (three women and seven men), ranging in age from 29 to 79 years, affected by plaque-type psoriasis vulgaris, were treated with MEL. Biopsies from psoriatic lesions of MEL-treated sites were taken before, 24 h and/or 48 h after the first irradiation and analysed by the immunophosphatase alkaline technique (APAAP).
MEL treatment was found to cause a significant decrease in the rate of proliferation of keratinocytes and a relevant depletion of T cells in all psoriatic lesions, 48 h after the first irradiation: 308 nm light eliminated T cells from the psoriatic epidermis and also from the dermis, highlighting the ability of this UVB source to penetrate the skin compared with normal UVB and establish direct cytotoxic action on T cells infiltrating skin lesions. Rapid clearing of psoriatic lesions involves potential molecular targets of UVB in T cells including p53, which is upregulated after direct irradiation with 308-nm UVB. Moreover, Bcl-2 expression in healing psoriasis epidermis after MEL treatment is significantly decreased compared with untreated skin and the TUNEL (TdT-mediated dUTP-biotin nick end labelling) technique revealed the presence of relevant apoptotic keratinocytes in the irradiated epidermis.
These results indicate that psoriatic skin after monochromatic excimer light therapy is associated with significant T-cell depletion and alterations of apoptosis-related molecules accompanied by a decreased proliferation index and clinical remission.
多种类型的中波紫外线(UVB)辐射源(290 - 320纳米)被用于治疗银屑病,其治疗机制归因于免疫抑制特性。最近,一种由308纳米准分子激光产生的新型UVB源已被引入用于银屑病的治疗。
在本研究中,我们调查了用308纳米单色准分子光(MEL)治疗前后银屑病增生性皮肤中T细胞的免疫组织化学评估以及各种凋亡相关分子的表达。
10例(3名女性和7名男性)年龄在29至79岁之间的寻常型斑块状银屑病患者接受了MEL治疗。在首次照射前、照射后24小时和/或48小时采集MEL治疗部位银屑病皮损的活检组织,并通过免疫碱性磷酸酶技术(APAAP)进行分析。
发现MEL治疗在首次照射后48小时导致所有银屑病皮损中的角质形成细胞增殖率显著降低以及T细胞明显减少:308纳米光使银屑病表皮和真皮中的T细胞消失,突出了这种UVB源与普通UVB相比穿透皮肤并对浸润皮损的T细胞产生直接细胞毒性作用的能力。银屑病皮损的快速消退涉及UVB在T细胞中的潜在分子靶点,包括p53,在用308纳米UVB直接照射后其表达上调。此外,与未治疗的皮肤相比,MEL治疗后愈合的银屑病表皮中Bcl - 2表达显著降低,并且TUNEL(末端脱氧核苷酸转移酶介导的dUTP - 生物素缺口末端标记)技术显示照射后的表皮中存在相关的凋亡角质形成细胞。
这些结果表明,单色准分子光治疗后的银屑病皮肤与显著的T细胞减少以及凋亡相关分子的改变相关,同时伴有增殖指数降低和临床缓解。