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Exposure to UVB Induces Accumulation of LFA‐1 + T Cells and Enhanced Expression of the Chemokine Psoriasin in Normal Human Skin ¶
Author(s) -
Nuzzo Sergio,
SylvaSteenland Regien M. R.,
Koomen Cornelis W.,
Rie Menno A.,
Das Pranab K.,
Bos Jan D.,
Teunissen Marcel B. M.
Publication year - 2000
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2000)0720374etuiao2.0.co2
Subject(s) - dermis , downregulation and upregulation , chemokine , cell adhesion molecule , microbiology and biotechnology , messenger rna , chemistry , icam 1 , human skin , biology , immunology , immune system , biochemistry , genetics , anatomy , gene
Normal human skin shows preferential (epi)dermal infiltration of CD4 + T cells upon acute UV exposure. To study the mechanism behind this feature we locally exposed healthy volunteers to doses of UV commonly encountered by the population. Expression of integrins on T cells and expression of adhesion molecules on dermal endothelial cells were quantitatively assessed by immunohistochemistry in situ. We also investigated the effects of ultraviolet‐B (UVB) exposure on psoriasin and IL‐16, two specific chemoattractant factors for CD4 + T cells, at messenger RNA (mRNA) level by semiquantitative reverse transcriptase‐polymerase chain reaction and at protein level by immunohistochemistry. We found, at day 2 after exposure to four minimal erythema doses of UVB, predominant accumulation of LFA‐1 + /CLA − /VLA‐4 − T cells in the dermis. Concomitantly the expression of ICAM‐1, but not that of E‐selectin and VCAM‐1, was upregulated on dermal endothelial cells. The increase in the number of dermal T cells was not due to proliferation because only 2% of the UVB‐induced dermal T cells expressed the marker of proliferation Ki‐67. Whereas exposure to 35 J/cm 2 of ultraviolet‐A (UVA), like UVB, induced a loss of intraepidermal T cells at day 2 after exposure, UVA induced neither any influx of T cells into the dermis nor any adhesion molecule upregulation on endothelial cells. In response to UVB exposure, the expression of psoriasin mRNA, but not of IL‐16 mRNA, was upregulated; the expression of psoriasin protein was also found to be upregulated. These results suggest that LFA‐1/ICAM‐1 pathway and psoriasin are both involved in the accumulation of CD4 + T cells into UVB‐irradiated skin, possibly via a recruitment mechanism.