Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease, in which sunlight (especially its ultraviolet radiation (UVR)) is known to induce exacerbate this condition. The focus of this paper is to investigate the
of cutaneous lesions as well as systemic manifestations of the disease. The aim of this in vitro study was toinvestigate 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 normalmice from the non-SLE strains (C57BL=6, BALB/c). Our results demonstrate the following. Dermal fibroblast of premorbid SLE mice showed increased susceptibility toUVA and UVB irradiation, determined by viability assay, incomparison to those of normal mice. UVB irradiation inducedan 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-inflammaory cytokines (IL-1, IL-6, TNF-a) in DF o premorbid SLE mice, in comparison to normal controls. Theenhanced pro-inflammatory responses to UVR werealsoobserved in experiments conducted with cells derivedfrom morbid SLE mice.
In conclusion, the pro-inflammatory pronenessdetected in the premorbid stage of murine SLE could be ofmajor importance in SLE pathogenesis. Furthermore, it suggests that the autoimmine inflammatory process in vivo, triggered initially by immune complex deposition, could be further amplified by UVR.
Normally, the immune system helps protect the body from harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. The result is an overactive immune response that attacks otherwise healthy cells...