Department of Medicine and Therapeutics and the Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong (CUHK), Shatin, Hong Kong, China.
J Rheumatol. 2012 Oct;39(10):1942-7. doi: 10.3899/jrheum.120177. Epub 2012 Aug 15.
To study the role of tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK)/Fn14 and the interferon-inducible protein (IP-10)/CXCR3 axis in lupus nephritis (LN).
We studied 113 patients with LN who had had repeat renal biopsies. Glomerular and tubulointerstitial messenger RNA expression of TWEAK, Fn14, IP-10, and CXCR3 were quantified.
Glomerular Fn14 expression decreased when changed from proliferative or mixed nephritis to membranous nephropathy (p = 0.016), and increased when changed from membranous to proliferative or mixed nephritis (p = 0.0006). On the other hand, tubulointerstitial TWEAK expression decreased when changed from proliferative or mixed nephritis to membranous nephropathy (p = 0.004), and increased when changed from membranous nephropathy to proliferative nephritis (p = 0.010). Tubulointerstitial IP-10 expression decreased when changed from proliferative or mixed nephritis to membranous nephropathy (p < 0.0001). Histological activity index correlated significantly with the glomerular expression of Fn14 (r = 0.421, p < 0.0001) and tubulointerstitial expression of TWEAK (r = 0.413, p < 0.0001) and IP-10 (r = 0.472, p < 0.0001).
Glomerular Fn14 and tubulointerstitial TWEAK and IP-10 expression appeared to have consistent changes in relation to the histological class of LN and correlated with the histological activity index. Our findings suggest a specific role of these genes in the pathogenesis of LN.
研究肿瘤坏死因子(TNF)样凋亡弱诱导物(TWEAK)/Fn14 和干扰素诱导蛋白(IP-10)/CXCR3 轴在狼疮肾炎(LN)中的作用。
我们研究了 113 例重复肾活检的 LN 患者。定量分析了 TWEAK、Fn14、IP-10 和 CXCR3 的肾小球和肾小管间质信使 RNA 表达。
肾小球 Fn14 表达从增生性或混合性肾炎变为膜性肾炎时减少(p = 0.016),从膜性肾炎变为增生性或混合性肾炎时增加(p = 0.0006)。另一方面,肾小管间质 TWEAK 表达从增生性或混合性肾炎变为膜性肾炎时减少(p = 0.004),从膜性肾炎变为增生性肾炎时增加(p = 0.010)。肾小管间质 IP-10 表达从增生性或混合性肾炎变为膜性肾炎时减少(p < 0.0001)。组织学活动指数与肾小球 Fn14 表达(r = 0.421,p < 0.0001)和肾小管间质 TWEAK 表达(r = 0.413,p < 0.0001)和 IP-10 表达(r = 0.472,p < 0.0001)显著相关。
肾小球 Fn14 和肾小管间质 TWEAK 和 IP-10 的表达似乎与 LN 的组织学类型有一致的变化,并与组织学活动指数相关。我们的发现表明这些基因在 LN 的发病机制中具有特定作用。