Exposure to UVB induces accumulation of LFA-1(+) T cells and enhanced expression of the chemokine psoriasin in normal human skin

Normal human skin shows preferential (epi)dermal infiltration of CD4(+) T c ells upon acute UV exposure. To study the mechanism behind this feature we locally exposed healthy volunteers to doses of UV commonly encountered by t he population. Expression of integrins an T cells and expression of adhesio n molecules on dermal endothelial cells were quantitatively assessed by imm unohistochemistry in situ, We also investigated the effects of ultraviolet- B (UVB) exposure on psoriasin and IL-16, two specific chemoattractant facto rs for CD4(+) T cells, at messenger RNA (mRNA) Level by semiquantitative re verse transcriptase-polymerase chain reaction and at protein level by immun ohistochemistry. We found, at day 2 after exposure to four minimal erythema doses of UVB, predominant accumulation of LFA-1(+)/CLA(-)/VLA-4(-) cells i n the dermis. Concomitantly the expression of ICAM-1, but not that of E-sel ectin and VCAM-1, was upregulated an 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, ind uced 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 upr egulation on endothelial cells, Ln 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 sugges t that LFA-1/ICAM-1 pathway and psoriasin are both involved tn the accumula tion of CD4(+) T cells into UVB-irradiated skin. possibly I ia a recruitmen t mechanism.