Langerhans cells that migrate to skin after intravenous infusion regulate the induction of contact hypersensitivity.

Intravenous infusion of hapten-derivatized epidermal cells (EC) in syngeneic mice leads to two competing signals for contact hypersensitivity (CH), a dominant effector signal attributable to Langerhans cells (LC) and a suppressor signal from Thy-1+ EC. In vitro exposure of LC to low dose ultraviolet B (UVB) radiation before hapten-derivatization and infusion not only results in the abrogation of their effector signal but also causes the down-regulation of subsequent CH responses. To delineate the relevance of i.v. immunization to the study of CH and of LC as the immunologic targets of low dose UVB radiation, we examined the migratory and immunogenic properties of EC after i.v. infusion. Unsorted EC migrated from blood to skin and lymphoid tissues, reaching steady state distributions at 16 h after infusion. No significant differences were observed between the trafficking of EC in syngeneic and allogeneic transfers. LC localized preferentially to skin, whereas Thy-1+ EC trafficked to skin, the thymus, mesenteric lymph nodes, and spleen. The pattern of trafficking of unirradiated and low dose UVB-irradiated LC were identical, suggesting that low dose UVB radiation had little effect on LC migration. Finally, skin graft experiments demonstrated i.v. infused, hapten-derivatized LC that migrate to skin to retain their capacity to induce CH, a property that was converted by in vitro pretreatment with low dose UVB radiation into down-regulation. These findings confirm the relevance and utility of the i.v. immunization model in the study of CH and the influence of low dose UVB on this immune response. Our data also provide a basis for investigating the role of disparate trafficking patterns in generating effector and suppressor signals when hapten-derivatized EC are employed for CH.