Rood M J, Keijsers V, van der Linden M W, Tong T Q, Borggreve S E, Verweij C L, Breedveld F C, Huizinga T W
Department of Rheumatology, Leiden University Medical Centre, The Netherlands.
Ann Rheum Dis. 1999 Feb;58(2):85-9. doi: 10.1136/ard.58.2.85.
To investigate the association of interleukin 10 (IL10) promoter polymorphisms and neuropsychiatric manifestations of systemic lupus erythematosus (SLE).
IL10 haplotypes of 11 healthy volunteers were cloned to confirm that in the Dutch population, only the three common haplotypes (-1082/-819/-592) GCC, ACC and ATA exist. The IL10 promoter polymorphisms of 92 SLE patients and 162 healthy controls were determined. The medical records of the SLE patients were screened for the presence of neuropsychiatric involvement.
All cloned haplotypes were either GCC, ACC or ATA. Forty two SLE patients had suffered from neuropsychiatric manifestations (NP-SLE). In NP-SLE patients, the frequency of the ATA haplotype is 30% versus 18% in the controls and 17% in the non-NP-SLE group (odds ratios 1.9, p = 0.02, and 2.1, p = 0.04, respectively), whereas the GCC haplotype frequency is lower in the NP-SLE group compared with controls and non-NP-SLE patients (40% versus 55% and 61%, odds ratios 0.6, p = 0.02 and 0.4 p = 0.006). The odds ratio for the presence of NP-SLE is inversely proportional to the number of GCC haplotypes per genotype when the NP-SLE group is compared with non-NP-SLE patients.
The IL10 locus is associated with neuropsychiatric manifestations in SLE. This suggests that IL10 is implicated in the immunopathogenesis of neuropsychiatric manifestations in SLE.
研究白细胞介素10(IL10)启动子多态性与系统性红斑狼疮(SLE)神经精神症状之间的关联。
克隆11名健康志愿者的IL10单倍型,以确认在荷兰人群中仅存在三种常见单倍型(-1082/-819/-592)GCC、ACC和ATA。测定92例SLE患者和162名健康对照者的IL10启动子多态性。筛查SLE患者的病历以确定是否存在神经精神受累情况。
所有克隆的单倍型均为GCC、ACC或ATA。42例SLE患者出现神经精神症状(NP-SLE)。在NP-SLE患者中,ATA单倍型的频率为30%,而对照组为18%,非NP-SLE组为17%(优势比分别为1.9,p = 0.02和2.1,p = 0.04),而NP-SLE组的GCC单倍型频率低于对照组和非NP-SLE患者(40%对55%和6%)。与非NP-SLE患者相比,NP-SLE组中NP-SLE存在的优势比与每个基因型中GCC单倍型的数量成反比。
IL10基因座与SLE的神经精神症状相关。这表明IL10参与了SLE神经精神症状的免疫发病机制。