1994British Journal of DermatologyRequires access

Immunohistochemical study of desmosomes in acne vulgaris

H. Knaggs, B.R. HUGHES, Christopher J. Morris, Edward J. Wood, D.B. Holland, W.J. Cunliffe

Open publisher page 24 citations

Abstract

Desmosomes contribute towards adhesion between adjacent keratinocytes. In acne vulgaris, increased intercellular adhesion is thought to contribute to the retention of keratinocytes within the follicular lumen during comedogenesis. Therefore, the distribution of different desmosomal components was investigated in normal and acne subjects. Biopsies were cryostat-sectioned (6 microns), and stained with antibodies to different desmosomal components: desmoplakin 1/2, desmoglein 1, desmocollin 3a/3b, and a late desmosomal antigen, G36-19. Desmoplakin 1/2, desmoglein 1 and desmocollin 3a/3b shared a similar distribution in follicles from control skin, from acne-affected skin, and in non-inflamed lesions. All three proteins were expressed around the periphery of keratinocytes of all the intrafollicular epidermis, except the basal lamina and the upper stratum corneum. In inflamed lesions, the expression of desmoglein 1 and desmocollin 3a/3b was diminished; in 12.5%, staining for these two proteins was completely abolished, and in 81.25% of the lesions 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 epithelia of controls, non-inflamed, and inflamed lesions. This study, using monoclonal antibodies, did not identify any changes in the desmosomal components which might explain the increased adhesion between follicular keratinocytes during comedogenesis.

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What this paper is about

Desmosomes contribute towards adhesion between adjacent keratinocytes. In acne vulgaris, increased intercellular adhesion is thought to contribute to the retention of keratinocytes within the follicular lumen during comedogenesis. Therefore, the distribution of different desmosomal components was investigated in normal and acne subjects. Biopsies were cryostat-sectioned (6 microns), and stained with antibodies to different desmosomal components: desmoplakin 1/2, desmoglein 1, desmocollin 3a/3b, and a late desmosomal antigen, G36-19. Desmoplakin 1/2, desmoglein 1 and desmocollin 3a/3b shared a similar distribution in follicles from control skin, from acne-affected skin, and in non-inflamed lesions. All three proteins were expressed around the periphery of keratinocytes of all the intrafollicular epidermis, except the basal lamina and the upper stratum corneum. In inflamed lesions, the expression of desmoglein 1 and desmocollin 3a/3b was diminished; in 12.5%, staining for these two proteins was completely abolished, and in 81.25% of the lesions 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 epithelia of controls, non-inflamed, and inflamed lesions. This study, using monoclonal antibodies, did not identify any changes in the desmosomal components which might explain the increased adhesion between follicular keratinocytes during comedogenesis.

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Available abstract

Desmosomes contribute towards adhesion between adjacent keratinocytes. In acne vulgaris, increased intercellular adhesion is thought to contribute to the retention of keratinocytes within the follicular lumen during comedogenesis. Therefore, the distribution of different desmosomal components was investigated in normal and acne subjects. Biopsies were cryostat-sectioned (6 microns), and stained with antibodies to different desmosomal components: desmoplakin 1/2, desmoglein 1, desmocollin 3a/3b, and a late desmosomal antigen, G36-19. Desmoplakin 1/2, desmoglein 1 and desmocollin 3a/3b shared a similar distribution in follicles from control skin, from acne-affected skin, and in non-inflamed lesions. All three proteins were expressed around the periphery of keratinocytes of all the intrafollicular epidermis, except the basal lamina and the upper stratum corneum. In inflamed lesions, the expression of desmoglein 1 and desmocollin 3a/3b was diminished; in 12.5%, staining for these two proteins was completely abolished, and in 81.25% of the lesions 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 epithelia of controls, non-inflamed, and inflamed lesions. This study, using monoclonal antibodies, did not identify any changes in the desmosomal components which might explain the increased adhesion between follicular keratinocytes during comedogenesis.

Key concepts: Desmosome, Desmoplakin, Desmoglein 1, Desmoglein, Desmoglein 3, Pathology, Epidermis (zoology), Pemphigus vulgaris

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