Disparate effects of in vitro low-dose UVB irradiation on intravenous immunization with purified epidermal cell subpopulations for the induction of contact hypersensitivity

Low-dose ultraviolet (UV) B irradiation suppresses contact hypersensitivity (CH) reactions and alters the antigen presenting function of epidermal cells (EC) in mice. To identify the EC sources of immunosuppression in this system, we examined the effect of UVB on the capacity of EC to induce and to regulate CH to trinitrochlorobenzene (TNCB). On day 0, cell sorter-purified populations of Ia⁺EC, Thy-1⁺EC, or Ia^-/Thy-1^-EC from CBA and C3H/HeJ mice were exposed to 200 J/m² UVB from unfiltered FS20 Sunlamps, derivatized with hapten, and inoculated intravenously into syngeneic mice (5000 cells per inoculum). After 6 d, responsiveness was tested by challenging the left ear with 2% TNCB and measuring ear swelling responses. On day 14, regulation was tested by painting 7% TNCB on abdominal skin; after 6 d the right ear was challenged. Whereas mice which received haptenated unirradiated Ia⁺EC exhibited full CH responses without down-regulation, mice inoculated with haptenated irradiated Ia⁺EC displayed significantly diminished primary responses and, on subsequent immunization, displayed down-regulation. On the other hand, panels of mice that received haptenated unirradiated Thy-1⁺EC, and haptenated irradiated Thy-1⁺EC both showed hyporesponsiveness as well as down-regulation. Intravenous immunization with haptenated unirradiated Ia^-/Thy-1^-EC or with haptenated irradiated Ia-/Thy-1^-EC led in each instance to immunologically "null events". These findings indicate that UVB irradiation profoundly affected Ia⁺EC such that their capacity to sensitize for CH was not only abrogated, but that such treatment also resulted in down-regulation of CH responses. By contrast, the same phototreatment had no effect on the inherent property of Thy-1⁺EC to mediate down-regulation of CH. We conclude that Ia⁺EC are immunologically relevant targets of low-dose UVB radiation, and that two populations of irradiated EC, Ia⁺EC, and Thy-1⁺EC, have the potential to deliver down-regulatory signals in this model of immunosuppression.