The functional disruption of Langerhans cells (LC) by UVB radiation is involved in antigen-specific immunosuppression of contact hypersensitivity. We tested whether UVB radiation inhibits the endocytotic activity of LC, which leads to impaired subsequent migration and maturation. Human monocyte-derived LC that took up lucifer yellow (L Y) or FITC-dextran (Fd) exclusively migrated in response to 6Ckine and matured. Exposing LC to 10-40 mJ/cm$^2$ of UVB radiation reduced their endocytotic activity in fluid phase pinocytosis (measured by uptake of LY) and in receptor-mediated endocytosis (measured by uptake of Fd). Membrane ruffling and CD32 expression were also suppressed by UVB radiation. UVB-irradiated, endocytosing LC had less movement towards 6Ckine, expressed less CD54 and CD86, and had less effective stimulatory activity in allo-MLR than nonirradiated, endocytosing LC. Endocytosis up-regulated TNF-$alpha$ production by LC, but prior UVB radiation inhibited this enhancement. The finding that impaired endocytosis of LC by UVB radiation inhibits subsequent migration and maturation was also confirmed in murine epidermal cells obtained from unirradiated and 2OmJ/cm$^2$ of UVB-irradiated skin.