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/cm² 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.