Suppression of contact hypersensitivity in mice by ultraviolet irradiation is associated with defective antigen presentation.

A single dose of radiation from FS40 sunlamps results in systemic depression of delayed-type hypersensitivity (DTH) to 2-chloro-1,3,5-trinitrobenzene (TNCB) and 1-fluoro-2,4-dinitrobenzene (DNFB). Immunosuppression is proportional to the log10 dose of radiation and exhibits a delayed time course. Animals sensitized one day after ultraviolet (u.v.) treatment respond normally, but sensitization 3-15 days after treatment results in about 70% suppression of the DTH response. The dose response of DTH in normal and u.v.-treated animals to 1,3,5-trinitrophenyl (TNP) conjugated adherent splenocytes from normal or u.v.-treated donors was investigated. When normal mice were immunized with TNP-conjugated adherent splenocytes from normal or u.v.-treated donors, a DTH response could be elicited in these animals by injection of TNP-conjugated splenocytes into the ear. However, u.v.-irradiated recipients could not be sensitized by TNP-conjugated adherent cells from u.v.-treated mice but were sensitized by such cells from normal mice. Lysed, TNP-conjugated, normal adherent splenocytes did not immunize u.v.-irradiated recipients, but did immunize normal recipients. These results confirmed that antigen presentation is deficient in u.v.-treated mice. The time of appearance of the antigen-presenting defect in the spleen cells of u.v.-treated mice was the same as for the depression of contact sensitivity, strengthening the evidence for a causal relationship between defective antigen presentation and depression of contact sensitivity.