IMMUNOHISTOCHEMICAL STUDY OF DESMOSOMES IN ACNE-VULGARIS

Citation
He. Knaggs et al., IMMUNOHISTOCHEMICAL STUDY OF DESMOSOMES IN ACNE-VULGARIS, British journal of dermatology, 130(6), 1994, pp. 731-737
Citations number
35
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
00070963
Volume
130
Issue
6
Year of publication
1994
Pages
731 - 737
Database
ISI
SICI code
0007-0963(1994)130:6<731:ISODIA>2.0.ZU;2-P
Abstract
Desmosomes contribute towards adhesion beween adjacent keratinocytes. In acne vulgaris, increased intercellular adhesion is thought to contr ibute to the retention of keratinocytes within the follicular lumen du ring comedogenesis. Therefore, the distribution of different desmosoma l components was investigated in normal and acne subjects. Biopsies we re cryostat-sectioned (6 mu m), and stained with antibodies to differe nt desmosomal components: desmoplakin 1/2, desmoglein 1, desmocollin 3 a/3b, and a late desmosomal antigen, G36-19. Desmoplakin 1/2, desmogle in I and desmocollin 3a/3b shared a similar distribution in follicles from control skin, from acne-affected skin, and in noninflamed lesions . All three proteins were expressed around the periphery of keratinocy tes of all the intrafollicular epidermis, except the basal lamina and the upper stratum corneum. In inflamed lesions, the expression of desm oglein 1 and desmocollin 3a/3b was diminished; in 12.5%, staining for these two proteins was completely abolished, and in 81.25% of the lesi ons investigated the staining was patchy. The antibody G36-19 bound to an antigen in the upper granular layer in the infundibular epidermis. No differences were noted in the staining pattern of the follicular e pithelia of controls, non-inflamed, and inflamed lesions. This study, using monoclonal antibodies, did not identify any changes in the desmo somal components which might explain the increased adhesion between fo llicular keratinocytes during comedogenesis.