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.