Epidermal langerhans cell depletion after artificial ultraviolet B irradiation of human skin in vivo: apoptosis versus migration.
Ultraviolet B radiation can suppress cellular immunity. One of the mechanisms related to this immunosuppression is the disappearance of Langerhans cells from the epidermis. The aim of this study was to establish the mechanism of ultraviolet B-induced Langerhans cell disappearance in healthy individuals. The two most likely mechanisms for Langerhans cell disappearance are apoptosis and migration. Apoptosis was assessed in vivo by exposing buttock skin of 10 healthy volunteers to six minimal erythema doses of ultraviolet B. Only very few apoptotic Langerhans cells could be observed in sections from the ultraviolet B-exposed skin. Migration of Langerhans cells cannot be established in skin sections and suction blisters were therefore raised in an attempt to trap migrating Langerhans cells in the sub-basal membrane blister fluid. Blisters were raised on the flexor side of the lower arm of 30 healthy volunteers at several time points after exposure of the skin to six minimal erythema doses of ultraviolet B. Blister fluid was collected and blister roofs were removed to check for Langerhans cell disappearance. Langerhans cells were detected in the blister fluid of the ultraviolet B-exposed skin and not of the unexposed skin. The number of Langerhans cells in the blister fluid peaked at about 18 h after ultraviolet exposure, which coincided with the largest depletion of Langerhans cells in the blister roof. A fraction (20-30%) of the Langerhans cells in the blister fluid stained positive for DNA damage (cyclobutyl pyrimidine dimers), showing that they originated from the epidermis. Ultraviolet B-induced Langerhans cell disappearance appears to be mainly attributable to migration.
Kölgen
Wendy
W
Department of Dermatology, University Medical Center Utrecht, Utrecht, the Netherlands. w.kolgen@azu.nl
Both
Hilde
H
van Weelden
Huib
H
Guikers
Kees L H
KL
Bruijnzeel-Koomen
Carla A F M
CA
Knol
Edward F
EF
van Vloten
Willem A
WA
De Gruijl
Frank R
FR
D000328:Adult; D018949:Antigens, CD1 / Q000032:analysis; D017209:Apoptosis / Q000276:immunology*; D001768:Blister / Q000473:pathology; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002465:Cell Movement / Q000276:immunology*; D004249:DNA Damage; D004817:Epidermis / Q000473:pathology* / Q000528:radiation effects; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D007801:Langerhans Cells / Q000737:chemistry / Q000473:pathology* / Q000528:radiation effects; D008297:Male; D008875:Middle Aged; D011740:Pyrimidine Dimers / Q000032:analysis; D013396:Suction; D014466:Ultraviolet Rays
D018949:Antigens, CD1; C419393:CD1a antigen; D011740:Pyrimidine Dimers; C059224:cyclobutyldithymidine dimers; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases