“…Redoules et al (1999) observed reduced activity of SC trypsin-like kallikreins in dry noneczematous AD skin (i.e., AX lesions). As this class of enzyme is essential for the degradation of desmoglein 1, its reduced activity may explain the increased number of SC cell layers reported by Tagami et al (2006) Equally, Tarroux et al (2002) demonstrated that its activity increases as the lesions are resolved. Conversely, Komatsu et al (2007) found increased mass levels of SC kallikreins together with plasmin and furin in mild lichenified AD lesions, which may be attributed to the decreased number of cell layers in AD lesions reported by White et al (1987) Equally, Hansson et al (2002) reported increased SCCE (KLK7) immunostaining in skin biopsies taken from AD subjects with chronic eczematous lesions on the flexural sides of the lower arms.…”