Zhao Jian, Wu Hui, Langefeld Carl D, Kaufman Kenneth M, Kelly Jennifer A, Bae Sang-Cheol, Alarcón Graciela S, Anaya Juan-Manuel, Criswell Lindsey A, Freedman Barry I, Kamen Diane L, Gilkeson Gary S, Jacob Chaim O, James Judith A, Merrill Joan T, Gaffney Patrick M, Sivils Kathy Moser, Niewold Timothy B, Petri Michelle A, Song Seung Taek, Jeong Hye-Jin, Ramsey-Goldman Rosalind, Reveille John D, Scofield R Hal, Stevens Anne M, Boackle Susan A, Vilá Luis M, Chang Deh-Ming, Song Yeong Wook, Vyse Timothy J, Harley John B, Brown Elizabeth E, Edberg Jeffrey C, Kimberly Robert P, Hahn Bevra H, Grossman Jennifer M, Tsao Betty P, La Cava Antonio
Department of Medicine, University of California Los Angeles, Los Angeles, CA, United States.
Department of Biostatistical Sciences and Center for Public Health Genomics, Wake Forest School of Medicine, Winston-Salem, NC, United States.
Clin Immunol. 2015 Dec;161(2):157-62. doi: 10.1016/j.clim.2015.09.007. Epub 2015 Sep 16.
Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE.
在系统性红斑狼疮(SLE)患者的血浆中,瘦素水平异常升高,据认为它会促进和/或维持促炎反应。这种关联是否反映了患SLE的遗传易感性增加尚不清楚,迄今为止,对SLE患者中与瘦素相关多态性的基因关联研究尚无定论。在这里,我们对来自四个不同祖先群体的15706名SLE患者和健康匹配对照的DNA样本进行了基因分型,以将瘦素途径基因的多态性与SLE风险相关联。结果发现,尽管有几个单核苷酸多态性(SNP)显示出微弱的关联,但在进行多重检验校正后,这些关联不再显著。这些数据不支持特定的瘦素相关多态性与患SLE易感性增加之间的关联。