Sasajima Tomomi, Watanabe Hiroshi, Sato Shuzo, Sato Yukio, Ohira Hiromasa
Fukushima Medical University, Department of Internal Medicine II, School of Medicine, Fukushima 960-1295, Japan.
J Neuroimmunol. 2006 Dec;181(1-2):150-6. doi: 10.1016/j.jneuroim.2006.09.003. Epub 2006 Oct 24.
We detected anti-triosephosphate isomerase antibodies (anti-TPI) in cerebrospinal fluid (CSF) in 5 of 12 neuropsychiatric lupus patients (41.6%) by Western blotting. C3d index was significantly higher in anti-TPI-positive patient (n=5, median 0.446) than in anti-TPI-negative patient (n=7, median 0.098) (p=0.019) CSF samples. TPI was detected from immune complexes (IC) isolated from CSF in 2 of 2 anti-TPI-positive patients tested and was not detected from IC in 5 of 5 anti-TPI-negative patients tested. Our results suggest that anti-TPI form IC in CSF and contribute to the pathogenesis of neuropsychiatric lupus by activating the complement system.
通过蛋白质印迹法,我们在12例神经精神性狼疮患者中的5例(41.6%)脑脊液(CSF)中检测到抗磷酸丙糖异构酶抗体(抗-TPI)。抗-TPI阳性患者(n=5,中位数0.446)的C3d指数显著高于抗-TPI阴性患者(n=7,中位数0.098)(p=0.019)的脑脊液样本。在检测的2例抗-TPI阳性患者中,从CSF分离的免疫复合物(IC)中检测到了TPI,而在检测的5例抗-TPI阴性患者中,IC中未检测到TPI。我们的结果表明,抗-TPI在CSF中形成IC,并通过激活补体系统促进神经精神性狼疮的发病机制。