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Expression of fetal cytokeratins in epidermai cells and colloid bodies in lichen planus *
Author(s) -
Biermann Heike,
Rauterberg Ernst W.
Publication year - 1998
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.1600-0560.1998.tb01687.x
Subject(s) - cytokeratin , pathology , immunohistochemistry , basal (medicine) , keratinocyte , epidermis (zoology) , biology , antigen , monoclonal antibody , keratin , antibody , staining , immunology , anatomy , medicine , cell culture , endocrinology , genetics , insulin
Clusters of immunoglobulin (Ig)‐coated colloid bodies (CBs) in the dermo‐epidermal zone are a typical immunohistochemical feature in lichen planus (LP)‐lesions. They are considered to represent dyskeratotic basal keratinocytes, yet their composition has not been completely elucidated. In the present study, skin biopsies of 10 LP‐lesions, 3 other dermatoses, and 10 biopsies of normal skin were studied immunohistochemically using monoclonal antibodies (MAbs) against fetal and differentiated epidermal antigens. CBs were identified by FITC‐anti‐Ig. Binding of MAb was visualized by double staining technique. Cytokeratin (CK) 10/11, a marker of epidermal differentiation, was consistently detected in suprabasal keratinocytes and also in up to 95% of Ig‐positive CBs in LP. CK10/11 was additionally detected in basal keratinocytes in 9 LP‐lesions, but not in normal skin. The basal cell‐specific MAb BL7 stained basal layer keratinocytes in all biopsies. In contrast to normal skin, in LP scattered suprabasal keratinocytes and CBs were also positive for BL7 in 10 and 7 cases, respectively. While fetal cytokeratins (CK13 and CK8/18) were completely absent in control skin specimens, both cytokeratins were detected in various numbers of keratinocytes and CBs in all LP‐lesions. Our results support the hypothesis of an epidermal origin of CBs. The cytokeratin profile seems to be severely disturbed in LP. This includes both accelerated differentiation by the expression of suprabasal CK10/11 in basal keratinocytes and dedifferentiation by the expression of fetal epidermal antigens (CK13 and CK8/18). It is tempting to speculate that the observed alterations may trigger T‐cell activation and inflammatory onset in LP.