Assessment of epidermal subpopulations and proliferation in healthy skin, symptomless and lesional skin of spreading psoriasis

Summary Background  The margin zone in spreading psoriatic lesions has frequently been used as a model to study the changes in epidermal proliferation, keratinization and inflammation during the transition from symptomless to lesional skin. However, the dynamics of the changes in the epidermal subpo...

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Published inBritish journal of dermatology (1951) Vol. 155; no. 4; pp. 688 - 694
Main Authors Körver, J.E.M., Van Duijnhoven, M.W.F.M., Pasch, M.C., Van Erp, P.E.J., Van De Kerkhof, P.C.M.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.10.2006
Blackwell
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Summary:Summary Background  The margin zone in spreading psoriatic lesions has frequently been used as a model to study the changes in epidermal proliferation, keratinization and inflammation during the transition from symptomless to lesional skin. However, the dynamics of the changes in the epidermal subpopulations—basal cells, transit amplifying cells and differentiated cells—have not been studied in the transition between symptomless and lesional skin. Objectives  To quantify in a dynamic model of the margin zone in psoriasis the characteristics of these subpopulations with respect to epidermal proliferation and differentiation. Methods  From seven patients with active psoriasis, biopsies were taken from the distant uninvolved skin, outer margin, inner margin and centre of a spreading psoriatic plaque. Frozen sections were labelled immunofluorescently using direct immunofluorescence for Ki‐67 and β1 integrin and the Zenon labelling technique for keratin 6, 10 and 15. Digital photographs of the stained sections were quantitatively analysed. Results  In the distant uninvolved skin the expression of β1 integrin was decreased and keratin 15 expression was lost. In this area suprabasal cells expressed β1 integrin and in the outer margin suprabasal cells expressed Ki‐67. From the outer to the inner margin of the psoriasis plaque, which coincided with the appearance of the clinical lesion, there was a significant change in the various markers. The patchy expression of keratin 6 in the inner margin became homogeneous in the centre of the psoriasis plaque and here was also coexpression of keratin 6 and keratin 10 in a single cell. Conclusions  The present study provides additional evidence that the distant uninvolved skin has a prepsoriatic phenotype, which is the first step in a psoriatic cascade. The cascade between symptomless and lesional skin comprises first an abnormality in inflammation with involvement of β1 integrin‐dim cells (transit amplifying cells) subsequently eliciting an enlarged germinative compartment with increased recruitment of cycling epidermal cells and focal expression of proliferation‐associated keratins, ultimately culminating in a more‐or‐less homogeneous epidermis with massive recruitment of cycling epidermal cells and proliferation‐associated keratinization.
Bibliography:ArticleID:BJD7403
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Conflicts of interest None declared.
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ISSN:0007-0963
1365-2133
DOI:10.1111/j.1365-2133.2006.07403.x