Alterations of immune functions in barrier disrupted skin by UVB irradiation.
BACKGROUND
While immunologic events elicited by acute barrier disruption or UVB irradiation have been studied in detail, the biological sequel of multiple insults to the skin is not well understood.


OBJECTIVE
Since the skin would receive a variety of simultaneous stimuli in daily life, we tested the effects of sequential treatments with barrier disruption and UVB exposure on skin immunity.


METHODS
Earlobes of BALB/c mice received tape-stripping and subsequently low-dose UVB exposure. Control mice were treated with either tape-stripping or UVB. The expression of surface markers and cytokine production in Langerhans cells and keratinocytes and the elicitation response of contact hypersensitivity were compared.


RESULTS
By flow cytometry, tape-stripping augmented the expression of MHC class II, CD54, CD80, CD86 and CD40 on Langerhans cells, whereas UVB decreased the expression of some of these molecules. Combination of tape-stripping and UVB induced largely intermediate levels between these two. Upon stimulation with L cells expressing CD40L, Langerhans cells from tape-stripped and UVB-irradiated earlobes strongly transcribed mRNA for interleukin-1beta compared to each treatment. In keratinocytes, tape-stripping or UVB slightly upregulated tumor necrosis factor-alpha and interleukin-1alpha production at both mRNA and protein levels, whereas these two treatments synergistically increased the production of these cytokines. The in vitro hapten-presenting ability of Langerhans cells to trinitrophenyl-immune lymph node T cells ranked first in tape-stripping, second in tape-stripping plus UVB and third in UVB, and so did the intensity of elicitation responses in contact hypersensitivity to a hapten, picryl chloride.


CONCLUSIONS
It is suggested that barrier disruption and UVB antagonize with each other in contact hypersensitivity as a reflection of their effects on Langerhans cell antigen-presenting function, but they synergize in cytokine production by both Langerhans cells and keratinocytes.
Ito
Taisuke
T
Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan.
Seo
Naohiro
N
Yagita
Hideo
H
Tsujimura
Kunio
K
Takigawa
Masahiro
M
Tokura
Yoshiki
Y
D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D003877:Dermatitis, Contact / Q000209:etiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D015870:Gene Expression; D005802:Genes, MHC Class II / Q000276:immunology / Q000528:radiation effects; D007375:Interleukin-1 / Q000032:analysis; D015603:Keratinocytes / Q000276:immunology / Q000528:radiation effects; D007801:Langerhans Cells / Q000276:immunology / Q000528:radiation effects; D051379:Mice; D008807:Mice, Inbred BALB C; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000276:immunology* / Q000293:injuries / Q000528:radiation effects*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014466:Ultraviolet Rays / Q000009:adverse effects*
D015703:Antigens, CD; D015415:Biomarkers; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha