Pelton B K, Hylton W, Denman A M
Division of Immunological Medicine, Northwick Park Hospital, Harrow, Middlesex, UK.
Clin Exp Immunol. 1992 Aug;89(2):251-4. doi: 10.1111/j.1365-2249.1992.tb06940.x.
Cultured mononuclear cells from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and normal donors were assayed for their ability to secrete IL-6 both spontaneously and after exposure to UV light. Mononuclear cells from SLE, RA and atopic control patients produced IL-6 spontaneously, while those from normal donors did not. Spontaneous production of IL-6 occurred in the non-adherent cell population. UV light-induced IL-6 production was confined exclusively to the SLE patients and was present only in the macrophage/monocyte fraction. This stimulation was induced by wavelengths in the UVA, UVB but not the UVC portion of the spectrum. These results suggest that cytokine release may be involved in the exacerbations of SLE provoked by photosensitivity.
对系统性红斑狼疮(SLE)患者、类风湿性关节炎(RA)患者以及正常供体的培养单核细胞,检测其自发分泌白细胞介素-6(IL-6)的能力以及暴露于紫外线后分泌IL-6的能力。来自SLE、RA患者和特应性对照患者的单核细胞可自发产生IL-6,而来自正常供体的单核细胞则不会。IL-6的自发产生发生在非贴壁细胞群体中。紫外线诱导的IL-6产生仅局限于SLE患者,且仅存在于巨噬细胞/单核细胞部分。这种刺激是由光谱中的UVA、UVB波段而非UVC波段的波长诱导的。这些结果表明,细胞因子释放可能参与了光敏性引发的SLE病情加重过程。