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系统性红斑狼疮(systemic lupus erythematosus,SLE)是以系统性、慢性、复发-缓解交替为特征的自身免疫性疾病典型代表,主要临床特点是血循环可检出大量自身抗体及多器官受损,其中神经精神性红斑狼疮(neuropsychiatric systemic lupus erythematosus,NPSLE)是常见并发症,患病率介于37%~95%之间,仅次于狼疮性肾炎,已成为影响SLE患者预后的主要因素之一[1]。目前NPSLE发病机制仍有很多未明之处,诊断与治疗仍面临很多挑战[2],加强NPSLE发病机制研究意义重大。本文将主要从神经免疫界面受损、免疫效应细胞、炎症因子、致病性自身抗体在NPSLE中发病作用研究进展及NPSLE研究常用动物模型进行综述,为阐明NPSLE发病机制和寻找研究靶点提供参考。 相似文献
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系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种病程反复、累及多种器官的自身免疫性疾病,其免疫学特征主要是高滴度的自身抗体和伴随抑制性T淋巴细胞减少的自身反应性B淋巴细胞增多,但机制尚未完全清楚. 相似文献
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<正>系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种可累及多种系统、原因不明的自身免疫性疾病。临床表现为血清中出现多种自身抗体,常累及肾脏,引起狼疮性肾炎,最后导致患者死亡[1]。据报道70%的SLE患者有肾脏受损的表现,引发狼疮性肾炎(lupus nephritis,LN),严重者可导致肾功能衰竭[2]。细胞因子异常分泌在SLE发病中发挥着 相似文献
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《细胞与分子免疫学杂志》2016,(8)
正系统性红斑狼疮(systemic lupus erythematosus,SLE)患者机体淋巴细胞功能失调,产生多种自身抗体,发病机制复杂[1]。维生素D属于类固醇激素,在血中主要形式是25羟基维生素D3[25(OH)VD3],在肾脏1α羟化酶作用下生成活性形式1,25二羟基维生素D3[1,25(OH)2VD3],1,25(OH)2VD3可通过淋巴细胞影响机体免疫系统[2-3]。由于25(OH) 相似文献
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系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种由于免疫系统紊乱导致机体产生多种自身抗体的自身免疫病。SLE发病缓慢,临床表现多样化,涉及多个系统和多种脏器损伤,造成细胞和体液免疫功能障碍,产生多种自身抗体。SLE的常见临床表现为发热、皮疹、关节痛、浆膜炎及肾、心血管、肺、神经系统、消化系统等系统损伤,死亡率高。虽然目前SLE发病的确切机制尚不清楚,但对于其发病原因比较公认的是核酸识别Toll样受体对于自身核酸复合物的识别而引发的针对自身的免疫反应。 相似文献
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系统性红斑狼疮(systemic lupus erythematosus,SLE)是多种因素相互作用引起的自身免疫性疾病,T细胞在其发生发展中发挥重要作用。近年来通过对SLE中T细胞的抗原特异性和克隆扩增特点的研究,发现SLE中T细胞识别特异性自身抗原,参与其发病的各个环节,并在SLE的病程持续中发挥重要作用。本文拟就有关内容作一综述。 相似文献
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Nancy P. Duarte-Delgado Gloria Vásquez Blanca L. Ortiz-Reyes 《Autoimmunity reviews》2019,18(4):426-432
Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease that can involve nervous system commitment known as neuropsychiatric systemic lupus erythematosus (NPSLE). The diagnostic of NPSLE is complex because the symptoms range from focal symptoms (e.g., strokes, thrombotic events) to diffuse disorders affecting cognition, mood and level of consciousness (e.g. acute confusional state, psychosis). Both type of manifestations of NPSLE differ in their pathological mechanisms. The focus of this review will be on the mechanisms that lead to the blood-brain barrier (BBB) disruption and to the neuroinflammation related with the diffuse manifestations of NPSLE. 相似文献
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Beatriz Lavras Costallat Daniel Miranda Ferreira Aline Tamires Lapa Letícia Rittner Lilian Tereza Lavras Costallat Simone Appenzeller 《Autoimmunity reviews》2018,17(1):36-43
Diffusion tensor imaging (DTI) maps the brain's microstructure by measuring fractional anisotropy (FA) and mean diffusivity (MD). This systematic review describes brain diffusion tensor Magnetic resonance imaging (MRI) studies in systemic lupus erythematosus (SLE).The literature was reviewed following the PRISMA guidelines and using the terms “lupus”, “systemic lupus erythematosus”, “SLE”, “diffusion tensor imaging”, “DTI”, “white matter” (WM), “microstructural damage”, “tractography”, and “fractional anisotropy”; the search included articles published in English from January 2007 to April 2017. The subjects included in the study were selected according to the ACR criteria and included 195 SLE patients with neuropsychiatric manifestation (NPSLE), 299 without neuropsychiatric manifestation (non-NPSLE), and 423 healthy controls (HC). Most studies identified significantly reduced FA and increased MD values in several WM regions of both NPSLE and non-NPSLE patients compared to HC. Subclinical microstructural changes were observed in either regional areas or the entire brain in both the non-NPSLE and NPSLE groups. 相似文献
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Psychiatric abnormalities are common in systemic lupus erythematosus (SLE) with a prevalence of 17% to 75%, reflecting different methods of patient selection and assessment, the different professional orientation of clinicians, and lack of an accepted consensus for diagnosing active neuropsychiatric lupus (NPSLE). The psychiatric syndromes included in the ACR Neuropsychiatric Lupus Nomenclature Committee criteria are cognitive dysfunction, acute confusional state (delirium), anxiety disorder, mood disorder, and psychosis. In SLE patients, identification of psychiatric phenomena and the generation of a differential diagnosis are crucial. Possible mechanisms include vascular injury and pathogenic antibodies. Treatment strategies are based on small case studies. The purpose of this review is to discuss clinical manifestations, pathogenesis and the present therapeutic options in psychiatric lupus. 相似文献
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Neuropsychiatric features of systemic lupus erythematosus 总被引:8,自引:0,他引:8
Borchers AT Aoki CA Naguwa SM Keen CL Shoenfeld Y Gershwin ME 《Autoimmunity reviews》2005,4(6):329-344
Neuropsychiatric systemic lupus erythematosus (NPSLE) is a serious and well known complication of systemic lupus erythematosus that remains a significant source of morbidity and mortality. Fortunately, advances in neuroimaging techniques and cognitive testing have improved the diagnosis of this disease and allowed earlier and more successful therapeutic intervention. Further, the association of NPSLE with the anti-phospholipid syndrome, other autoantibodies and inflammatory cytokines have also provided clues to the diagnosis and pathophysiology. Treatment of NPSLE is largely symptom based with outcome based on appropriate diagnosis. 相似文献
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《Autoimmunity reviews》2020,19(3):102463
The discovery of autoantibodies to ribosomal proteins (anti-RibP) dates back more than fifty years when antibodies to ribosomes were identified in systemic lupus erythematosus (SLE) sera. Over the years, anti-RibP autoantibodies have been the subject of extensive study and became known as a highly specific biomarker for the diagnosis of SLE and were associated with neuropsychiatric SLE (NPSLE), lupus nephritis (LN) and hepatitis (LH). As demonstrated by studies on cultured human cells and of murine models, there is evidence to suggest that anti-RibP may have a pathogenic role in LN and NPSLE. Despite a wealth of evidence, in comparison to other SLE autoantibodies such as anti-Sm and anti-dsDNA, anti-RibP has not been included in classification criteria for SLE. A significant challenge is the variability of assays used to detect anti-RibP, including the antigens and diagnostic platforms employed. This may account for the marked variation in frequencies (10–47%) in SLE and its association with clinical and demographic features reported in SLE cohorts. We performed a systematic literature review and meta-analysis to help clarify its prevalence, various clinical and serological associations in SLE based on the different RibP antigens and assay platforms used. 相似文献
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目的:探讨抗C1q 抗体及补体C3、C4 在神经精神性狼疮诊断中的应用价值。方法:对22 例狼疮脑病及66例SLE 患者进行横断面研究。抗C1q 抗体采用ELISA 方法,C3 及C4 采用免疫比浊法检测。分析补体与狼疮脑病的临床表现相关性,采用Logistic 回归分析狼疮脑病的危险因素。结果:NPSLE 患者抗C1q 抗体水平明显高于非NPSLE 患者,补体C4明显低于非NPSLE 患者,采用ROC 曲线分析抗C1q 抗体诊断NPSLE 敏感性及特异性分别为63.6%、66.7%。单因素分析后发现抗C1q 抗体、抗核糖体P 蛋白抗体、抗核小体抗体与神经精神性狼疮相关,但多因素Logistic 回归分析并未发现其与狼疮脑病发生有关。补体C4 降低与SLE 患者脑血管意外发生有关。结论:抗C1q 抗体在狼疮脑病诊断中具有一定的诊断价值,且补体C4 可能参与狼疮脑病脑血管意外的发生。 相似文献
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《Autoimmunity reviews》2014,13(9):963-973
Mouse models of autoimmunity, such as (NZB × NZW)F1, MRL/MpJ-Faslpr (MRL-lpr) and BXSB mice, spontaneously develop systemic lupus erythematosus (SLE)-like syndromes with heterogeneity and complexity that characterize human SLE. Despite their inherent limitations, such models have highly contributed to our current understanding of the pathogenesis of SLE as they provide powerful tools to approach the human disease at the genetic, cellular, molecular and environmental levels. They also allow novel treatment strategies to be evaluated in a complex integrated system, a favorable context knowing that very few murine models that adequately mimic human autoimmune diseases exist. As we move forward with more efficient medications to treat lupus patients, certain forms of the disease that requires to be better understood at the mechanistic level emerge. This is the case of neuropsychiatric (NP) events that affect 50–60% at SLE onset or within the first year after SLE diagnosis. Intense research performed at deciphering NP features in lupus mouse models has been undertaken. It is central to develop the first lead molecules aimed at specifically treating NPSLE. Here we discuss how mouse models, and most particularly MRL-lpr female mice, can be used for studying the pathogenesis of NPSLE in an animal setting, what are the NP symptoms that develop, and how they compare with human SLE, and, with a critical view, what are the neurobehavioral tests that are pertinent for evaluating the degree of altered functions and the progresses resulting from potentially active therapeutics. 相似文献
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Luis V C Portela Jo?o C T Brenol Roger Walz Marino Bianchin Adriano B L Tort Ubirajara P Canabarro Simone Beheregaray Jo?o A Marasca Ricardo M Xavier Eurico C Neto Carlos A Gon?alves Diogo O Souza 《Clinical and diagnostic laboratory immunology》2002,9(1):164-166
S100B is an astrocytic calcium-binding protein which has been proposed as a biochemical marker of brain damage or dysfunction in acute and chronic diseases. We investigated whether serum S100B levels could be related to systemic lupus erythematosus (SLE) activity. Patients were grouped as having inactive SLE (ISLE), active SLE without central nervous system (CNS) involvement (ASLE), or active SLE with unequivocal neurologic or psychiatric manifestation (NPSLE). The control group consisted of age- and sex-matched healthy blood donors. S100B levels were determined using a luminescence immunoassay. All SLE groups had higher levels of serum S100B than the control group. Among the SLE groups, significantly higher levels of serum S100B protein were found in the NPSLE group than in the ISLE and ASLE groups, and there was no significant difference in S100B levels between the ISLE and ASLE groups. These preliminary results point to a putative relevance of serum S100B protein levels in SLE patients, specifically concerning CNS involvement present in this disease. 相似文献