Objective: To investigate the involvement of type I interferons and endothelial cell adhesion molecules in the development of UVB-induced systemic lupus erythematosus skin lesions.
Methods: Nineteen SLE patients and 13 controls were irradiated with 2 Minimal Erythemal Doses (MED) of UVB. Subsequently, skin biopsies were analyzed (immuno)histologically, over 10 days, for expression of IFNα-induced MxA, numbers of plasmacytoid dendritic cells (pDC), and expression of endothelial cell adhesion molecules, namely, E-selectin, ICAM-1, and L-selectin ligand. Additionally, MxA expression was compared to its expression in 9 established cutaneous LE (CLE) lesions of SLE patients.
Results: Before irradiation IFNα-induced MxA was expressed at significantly higher levels in non-lesional skin of SLE patients compared to healthy controls. In patients developing infiltrates upon UVB irradiation, MxA expression increased further, reaching expression levels similar to or exceeding levels in CLE-skin lesions. In these patients, MxA expression was sustained up to day 10, in contrast to patients not developing infiltrates in whom expression decreased. No noteworthy numbers of plasmacytoid dendritic cells (pDC) were detected in non-irradiated skin or at any time after UVB exposure in SLE patients or controls. MxA expression correlated with influx of T-cells and monocytes/macrophages, and with expression of E-selectin and ICAM-1.
Conclusion: Development of UVB-induced SLE skin lesions involves a skewing towards production of Th1-associated cytokines, like IFNα. In turn, this may lead to upregulation of E-selectin and ICAM-1 resulting in recruitement of T-cells and macrophages.
- Interferon alpha
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