Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease, in which sunlight (especially its ultraviolet radiation (UVR)) is known to induce exacerbation of cutaneous lesions as well as systemic manifestations of the disease. The aim of this in vitro study was to investigate whether UVR (UVA, UVB) amplifies pro-inflammatory factors in cultured dermal fibroblasts (DF) or lymph node cells derived from premorbid or morbid mice from the murine SLE strains (MRL-1pr/1pr, (NZB/NZW)F1), in comparison to cells derived from normal mice from the non-SLE strains (C57BL/6, BALB/c). Our results demonstrate the following. Dermal fibroblast of premorbid SLE mice showed increased susceptibility to UVA and UVB irradiation, determined by viability assay, in comparison to those of normal mice. UVB irradiation induced an enhanced expression of ICAM-1 in such SLE derived cells, in comparison to cells of normal mice. UVA and UVB increased functional activity of LFA-1 in lymph node cells of premorbid SLE mice and not in normal controls. UVB irradiation induced increased production and secretion of pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha) in DF of premorbid SLE mice, in comparison to normal controls. The enhanced pro-inflammatory responses to UVR were also observed in experiments conducted with cells derived from morbid SLE mice. In conclusion, the pro-inflammatory proneness detected in the premorbid stage of murine SLE could be of major importance in SLE pathogenesis. Furthermore, it suggests that the autoimmune inflammatory process in vivo, triggered initially by immune complex deposition, could be further amplified by UVR.