1. Molecular Biology, AstraZeneca R&D, Mölndal, Sweden
2. ^*Molecular Biology, AstraZeneca R&D, Umeå, Sweden
3. ^‡AZ Transgenic Center, AstraZeneca R&D, Mölndal, Sweden
4. ^†Department of Public Health and Clinical Medicine, Section for Dermatology and Venereology, Umeå University, Umeå, Sweden

Correspondence: Dr Torbjörn Egelrud, Department of Public Health and Clinical Medicine; Dermatology and Venereology, University Hospital, SE-901 85 Umeå, Sweden. Email: torbjorn.egelrud@dermven.umu.se

¹Present address: Arexis AB, Krokslätts Fabriker 30, SE-43137, Mölndal, Sweden

²Present address: Department of Surgical and Perioperative Sciences, Sports Medicine Unit, Umeå University, SE-90185, Umeå, Sweden

³Present address: Swedish Defence Research Agency, SE-90182 Umeå, Sweden

⁴Present address: Bacterum AB, Glimmervägen 5E, SE-90740 Umeå, Sweden.

Received 24 April 2001; Revised 4 November 2001; Accepted 5 November 2001.

Abstract

Identification of tissue-specific mechanisms involved in the pathophysiology of inflammatory skin diseases could offer new possibilities to develop effective therapies with fewer systemic effects. The serine protease stratum corneum chymotryptic enzyme is preferentially expressed in cornifying epithelia. We have previously reported on increased expression of the stratum corneum chymotryptic enzyme in psoriasis. Here is reported an increased epidermal expression of stratum corneum chymotryptic enzyme also found in chronic lesions of atopic dermatitis. Transgenic mice expressing human stratum corneum chymotryptic enzyme in suprabasal epidermal keratinocytes were found to develop pathologic skin changes with increased epidermal thickness, hyperkeratosis, dermal inflammation, and severe pruritus. The results suggest that stratum corneum chymotryptic enzyme may be involved in the pathogenesis of inflammatory skin diseases, and that stratum corneum chymotryptic enzyme and related enzymes should be evaluated as potential targets for new therapies.