Effect of the H-2 and Igh complexes on the susceptibility to ultraviolet B-induced immunosuppression in murine contact sensitivity and contact photosensitivity.

We examined the genetic control of ultraviolet B (UVB)-induced immunosuppression in contact sensitivity (CS) to DNFB, picryl chloride, and oxazolone, and contact photosensitivity (CPS) to TCSA by using various H-2- and Igh-congenic strains. The CPS responses were inhibited by UVB preirradiation in all strains tested except for A/J mice, whereas only certain strains showed the immunosuppressive effect of UVB on the CS responses. In C.B-20 (H-2d, Igh-VbCb) and C3H (H-2k, Igh-VjCj) mice, the responses to 2-3 contact agents were suppressed by UVB pre-exposure. In C.AL-20 (H-2d, Igh-VdCd) mice, the UVB-induced suppression was observed in only 1 of the 3 CS systems. In contrast, BALB/c (H-2d, Igh-VaCa), BALB.B (H-2b, Igh-VaCa), BAB-14 (H-2d, Igh-VaCb), DBA/2 (H-2d, Igh-VcCc) and A/J (H-2a, Igh-VeCe) mice did not show immunosuppression in these CS systems. These data suggested that the susceptibility to UVB in the induction of cutaneous sensitivity depended on the mouse strain. There was no significant association between the susceptibility to UVB and the H-2 haplotype. However, the Igh complex partially contributed to UVB-induced suppression, as observed in a comparison of the CS responses between the Igh congenic strains, BALB/c, BAB-14 and C.B-20.