Ultraviolet radiation inhibits both accessory cell and responder T cell function in the proliferative response to haptenated-self.

Abstract

AbstractUltraviolet‐irradiated, hapten‐conjugated stimulator cells were unable to generate a proliferative response in unirradiated autologous T cells. The inhibition of the hapten‐specific response was found to depend on both the dose and waveband of UV radiation used as well as the timing of irradiation with regard to haptenation. UVC (254 nm) was 10‐fold more effective in eliminating the response than UVB (290–320 nm) which in turn was 104‐fold more effective than UVA (320–400 nm) with regard to the amount of incident energy required. Incident doses of UV lower than those within each waveband which virtually eliminated the response resulted in partial inhibition. This inhibition was significantly greater if UV radiation followed haptenation rather than preceding it, suggesting that UV radiation may have caused some loss of antigenicity. The interaction of UV radiation with hapten did not lead to enhanced phototoxicity; survival curves of viable cells placed in culture after the same dose and waveband of UV, either before, after or without haptenation, were similar. Independent experiments revealed that irradiation of the T cells with lower doses of UV than those required to reduce the stimulation 50% with irradiated haptenated stimulator cells, was itself directly inhibitory of their response to unirradiated, TNP‐conjugated adherent cells.