Sensitizing capacity of Langerhans' cells obtained from ultraviolet-B-exposed murine skin.

Acute low-dose ultraviolet B (UVB) radiation impairs contact hypersensitivity induction in some strains of mice (called UVB-susceptible, UVB-S), but not in others (called UVB-resistant, UVB-R). In order to determine whether these UVB-dependent phenotypes are inherent properties of epidermal Langerhans' cells, Ia-enriched epidermal cell suspensions were prepared from normal and UVB-exposed skin of C57BL/6 (UVB-S) and BALB/c (UVB-R) mice. After derivatization with dinitrofluorobenzene (DNFB), the cells were injected into footpads of naive syngeneic mice, and the recipients were evaluated for contact hypersensitivity and for in vitro evidence of hapten-specific T-cell priming. The results indicate that DNFB-conjugated Ia-enriched epidermal cells from normal mice, and from UVB-exposed skin of UVB-R mice induced contact hypersensitivity and primed hapten-specific T cells in the draining lymph node. By contrast, epidermal cells from UVB-exposed skin of UVB-S mice failed to induce contact hypersensitivity, even though hapten-specific T cells were still detectable in the draining lymph node. In addition, UVB radiation impaired the ability of hapten-bearing Langerhans' cells from UVB-S mice to activate hapten-specific, primed T cells in vitro. We conclude the traits of UVB-S and UVB-R can be expressed directly by Langerhans' cells, and that these effects are at least in part responsible for the deleterious consequences of UVB radiation on cutaneous immunity in UVB-S mice.