SUPPRESSION OF CONTACT HYPERSENSITIVITY IN MICE BY ULTRAVIOLET-IRRADIATION IS ASSOCIATED WITH DEFECTIVE ANTIGEN PRESENTATION

Abstract

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. Immunosuppression is proportional to the log10 dose of radiation and exhibits a delayed time course. Mice sensitized 1 day after UV treatment respond normally, but sensitization 3-15 days after treatment results in .apprx. 70% suppression of the DTH response. The dose response of DTH in normal and UV-treated animals to 1,3,5-trinitrophenyl (TNP) conjugated adherent splenocytes from normal or UV-treated donors was investigated. When normal mice were immunized with TNP-conjugated adherent splenocytes from normal or UV-treated donors, a DTH response could be elicited in these animals by injection of TNP-conjugated splenocytes into the ear. UV-irradiated recipients could not be sensitized by TNP-conjugated adherent cells from UV-treated mice but were sensitized by such cells from normal mice. Lysed, TNP-conjugated, normal adherent splenocytes did not immunize UV-irradiated recipients, but immunized normal recipients. Antigen presentation is apparently in UV-treated mice. The time of appearance of the antigen-presenting defect in the spleen cells of UV-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.