van Lingen R G, Poll M K P, Seyger M M B, de Jong E M G J, van de Kerkhof P C M, van Erp P E J
Department of Dermatology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
Arch Dermatol Res. 2008 Nov;300(10):561-7. doi: 10.1007/s00403-008-0862-1. Epub 2008 May 22.
The inflammation process in psoriatic skin is characterized by influx of leukocytes, hyperproliferation and aberrant differentiation of keratinocytes regulated via cytokines. Dipeptidyl-peptidase IV (DPPIV) is known to be upregulated on keratinocytes in the psoriatic lesion. The objective was to gain insight into dynamics of DPPIV expression and enzyme activity together with keratinocyte proliferation and differentiation markers during development of a psoriatic lesion, in order to investigate coherence in mechanisms behind the upregulation of DPPIV in psoriatic skin. The expression of DPPIV, Ki-67 antigen and keratin-16 (K16) was studied in the dynamic margin zone of the psoriatic lesion, examining skin sections of the clinically uninvolved skin, the early lesion and the chronic lesion of psoriatic patients compared to healthy volunteers using immunohistochemical and enzymehistochemical staining methods. DPPIV-expression and enzyme activity, Ki-67 antigen and K16 are significantly upregulated in the centre and inner margin of the lesion compared to clinically uninvolved skin and the healthy volunteers skin. Mutually between the centre and inner margin, this upregulation did not differ significantly. The clinical symptomless skin proved to have significantly elevated DPPIV enzyme activity compared to the skin of healthy volunteers. We demonstrate that DPPIV is expressed and enzymatically active well before the development of an overt psoriatic lesion. The abnormal DPPIV distribution in psoriatic skin does not coincide with known markers of aberrant growth and differentiation of keratinocytes, which makes DPPIV (expression and enzyme activity) a marker standing on its own.
银屑病皮肤的炎症过程的特征是白细胞流入、角质形成细胞的过度增殖和通过细胞因子调节的异常分化。已知二肽基肽酶IV(DPPIV)在银屑病皮损中的角质形成细胞上上调。目的是深入了解银屑病皮损发展过程中DPPIV表达和酶活性的动态变化以及角质形成细胞增殖和分化标志物,以研究银屑病皮肤中DPPIV上调背后机制的一致性。采用免疫组织化学和酶组织化学染色方法,研究了银屑病患者皮损动态边缘区、临床未受累皮肤、早期皮损和慢性皮损的皮肤切片中DPPIV、Ki-67抗原和角蛋白-16(K16)的表达,与健康志愿者进行比较。与临床未受累皮肤和健康志愿者皮肤相比,皮损中心和内边缘的DPPIV表达、酶活性、Ki-67抗原和K16显著上调。在中心和内边缘之间,这种上调没有显著差异。事实证明,与健康志愿者的皮肤相比,临床无症状皮肤的DPPIV酶活性显著升高。我们证明,在明显的银屑病皮损出现之前,DPPIV就已表达且具有酶活性。银屑病皮肤中DPPIV的异常分布与角质形成细胞异常生长和分化的已知标志物不一致,这使得DPPIV(表达和酶活性)成为一个独立的标志物。