Cutaneous exposure to low dose (2 kJ/m2) ultraviolet B radiation impairs the induction of contact hypersensitivity (CHS) responses to haptens applied to UV-irradiated skin and induces hapten-specific suppressor T lymphocytes (Ts). Cells collected from the draining lymph nodes of UV-irradiated, FITC-sensitized mice have impaired Ag-presenting activity and induce Ts cells upon injection into syngeneic recipients. This study investigates whether Ts cells originate in the UV-irradiated donor mice or are induced in lymph node cell recipients and the mechanism of suppression. Using congenic mice, we determined that the Ts cells in recipient animals were derived from T cells in the draining lymph nodes of the UV-irradiated donors. Cell lines and clones established from unirradiated and UV-irradiated, FITC-sensitized mice were CD4+, CD8-, TCR-alpha/beta+, MHC restricted, and hapten specific. The T cells proliferated in response to APC sensitized in vivo, but not to APC coupled in vitro with FITC. Cell lines from unirradiated mice were Th1 like, producing large amounts of IFN-gamma, but little IL-4 or IL-10, whereas cloned Ts cells from UV-irradiated mice produced IL-10, but no IL-4 or IFN-gamma. Ts cells blocked APC functions and IL-12 production in vitro. Injection of 5 x 10(4) cloned Ts cells into untreated recipients suppressed the induction of CHS. These results suggest that UV radiation can induce a distinct T regulatory type 1-like Ts population that may block the activation of Th1 cell-mediated immune responses.