Exposure of UVB-sensitive mice to immunosuppressive doses of UVB in vivo fails to affect the accessory function or the phenotype of draining lymph node dendritic cells.

Following the application of sensitizing chemicals to the skin, hapten-bearing Langerhans cells (LC) and possibly other cutaneous dendritic cells (DC) migrate to the draining lymph nodes (DLN) of mice and induce the proliferation of antigen specific effector T cells. This migration of DC to the DLN is required for the induction of primary immune responses. In certain strains of mice, irradiation with ultraviolet-B light (UVB) before sensitization results in the suppression of contact hypersensitivity responses. In vitro investigations have suggested that one influence of UVB is to modify the ability of Langerhans cells (LC) to present antigen. In the present investigation, putative UVB-induced alterations in lymph node DC in vivo were examined. Lymph node DC were analysed following exposure of C3H/HeN mice to an immunosuppressive dose of UVB (1440 J/m2) 48 and 24 h prior to skin painting with the sensitizers fluorescein isothiocyanate or oxazolone. In functional studies, DC prepared from the DLN of contact sensitized mice were examined for their ability to induce hapten-specific secondary T-lymphocyte proliferative responses or mixed lymphocyte reactions in vitro. In neither case was the activity of DC influenced by local exposure to an immunosuppressive dose of UVB. The migration of LC from the epidermis to the draining lymph node in response to contact sensitization is associated with increased expression of several membrane determinants necessary for effective antigen presentation, including intercellular adhesion molecule-1 (ICAM-1; CD54), B7-2 (CD86) and Ia antigen. The expression of these molecules was identical on DC isolated from the DLN of UVB-irradiated and from control, unirradiated mice. Thus, the immunosuppressive effect of UVB on the cutaneous immune system may not necessarily reflect changes in the antigen-presenting DC that accumulate in the DLN following skin sensitization.