Ultraviolet radiation (UVR)3 from within the spectrum B (UVB) has the capacity to distort the induction of contact hypersensitivity (CH) in murine skin. A damaging effect of UVB on epidermal Langerhans cells (LC) appears to be universal in all genetically defined strains of mice tested. However, while UVB impairs the induction of CH in some strains of mice, it has no apparent effect on CH in others. Thus, a disparity exists between the effects of UVB on LC and on CH. This is a paradox because LC are generally regarded to serve as the antigen-presenting cells of the skin, placing them at the earliest stages of induction of CH. One possible explanation for this paradox has been that UVB-susceptible strains of mice may generate hapten-specific suppressor T cells, whereas their UVB-resistant counterparts may not, when their skin is treated with UVR and painted with haptens such as dinitrofluorobenzene (DNFB). This possibility was excluded by examining the capacity of UVR and hapten to generate suppressor T cells in several different inbred strains of mice. The results indicate that the induction of hapten-specific afferent T suppressor cells is a universal sequela to treatment of mice with UVB and hapten, irrespective of whether the mice display the phenotype of vigorous CH or not. Thus, the genetic basis of UVB-resistance does not reside in the ability of UVR to induce suppressor T cells. Rather, attention should now be focused on its ability to interrupt induction of effector mechanisms.