Ultraviolet (UV) radiation to the whole body is known to cause selective systemic immunosuppression. Delayedtype hypersensitivity and contact hypersensitivity reactions are suppressed by UV radiation [8, 12, 13], although other general immune reactions, such as the mitogenic response, antibody formation, cytolytic T-cell induction and allograft rejection, are not affected [6, 9, 11]. Graft-versus-host disease (GVHD) is a complex process involving many different cell types and soluble mediators in immunoincompetent recipients after transfusion of allogeneic immunocompetent cells [5]. When normal F 1 hybrid mice, which are immunologically unresponsive to parental cells, are injected with parental strain lymphoid cells they develop transient GVHD, for example splenomegaly, but not lethal GVHD [2, 4]. In the present study, using this classical parent to F 1 GVHD model, we examined how in vivo UV irradiation, which is usually associated with suppression of immune responses, affects GVHD. Contrary to our expectation that UV would suppress GVHD, we found that UV enhanced GVHD. Female C57BL/6 (B6) (H-2 b) and (BALB/c x C57BL/6)F 1 (CB6F1) (H-2 b/d) mice were bred and maintained under pathogen-free conditions in the Experimental Animal Center, Kyoto University. All mice were used at 6-8 weeks of age. Systemic GVHD was induced in the CB6F 1 mice by intravenous injection of B6 spleen cells (5 x 107). As controls, CB6F1 mice were injected with syngeneic spleen cells. The dorsal hair of all CB6F 1 mice was shaved. Within 1 h of donor spleen cell injection, the recipient CB6F 1 mice were exposed for 1 h to UVB (280-320 nm) radiation emitted from a bank of five sunlamps (FL20S.E-30, Toshiba Electric, Tokyo, Japan). During irradiation, the