SLE患者血清中SARS-CoV抗体阳性原因分析

为了探讨严重急性呼吸综合征(SARS)冠状病毒(SARS-CoV)抗体测定在系统性红斑狼疮(SLE)患者中的假阳性问题,应用酶联免疫吸附试验(ELISA)和荧光定量RT-PCR技术检测了66例正常对照和31例SLE患者血清中SARS-CoV抗体的阳性率。结果,66例正常对照中,IgM抗体均阴性,IgG抗体的阳性率为3.0%(2/66);31例SLE患者中,IgM抗体和IgG抗体阳性率分别为29%(9/31)和58.1%(18/31),IgG抗体和IgM抗体同时阳性为22.6%(7/31)。经RTPCR检测,上述阳性病例均为阴性。结论:用非纯化抗原制备的ELISA试剂盒测定SLE患者的SARS-CoV抗体,可能出现假阳性,两种抗体同时测定可降低诊断的假阳性率,提高诊断的特异性。在SLE患者中出现假阳性的原因可能与包被的抗原有关。     

抗SmD1抗体对系统性红斑狼疮诊断的临床意义

目的探讨抗SmD1抗体的测定对系统性红斑狼疮(SLE)诊断的临床意义。方法用免疫学方法分别检测SLE患者90例、非SLE病例对照组患者100例及健康对照组患者70例血清中的自身抗体。抗SmD1抗体的检测用ELISA方法;抗Sm抗体、抗双链DNA(dsDNA)抗体、抗核小体抗体(ANuA)的检测用免疫印迹法。结果 SLE组患者血清中抗SmD1抗体阳性率为75.6%;抗ANuA抗体阳性率为56.7%;抗Sm抗体的阳性率为24.4%;抗dsDNA抗体阳性率为47.8%。SmD1抗体阳性率明显高于ANuA抗体、Sm抗体及dsDNA抗体,差异有统计学意义(P0.05),且抗SmD1抗体的特异性为98.2%。结论与传统的检测指标比较,抗SmD1抗体具有较高的敏感性和特异性,可作为诊断SLE的一项重要的特异性检测指标。     

SLE患者血清中SARS—CoV抗体阳性原因分析

为了探讨严重急性呼吸综合征(SARS)冠状病毒(SARS—CoV)抗体测定在系统性红斑狼疮(SLE)患者中的假阳性问题,应用酶联免疫吸附试验(ELISA)和荧光定量RT—PCR技术检测了66例正常对照和31例SLE患者血清中SARS—CoV抗体的阳性率。结果,66例正常对照中,IgM抗体均阴性,IgG抗体的阳性率为3．0％(2／66);31例SLE患者中,IgM抗体和IgG抗体阳性率分别为29％(9／31)和58．1％(18／31),IgG抗体和IgM抗体同时阳性为22．6％(7／31)。经RT—PCR检测,上述阳性病例均为阴性。结论：用非纯化抗原制备的ELISA试剂盒测定SLE患者的SARS—COV抗体,可能出现假阳性,两种抗体同时测定可降低诊断的假阳性率,提高诊断的特异性。在SLE患者中出现假阳性的原因可能与包被的抗原有关。     

CD154在活动期SLE的改变

目的探讨CD154在系统性红斑狼疮(SLE)中的异常表达及其在狼疮发病中的作用机制。方法31例活动期SLE及20例正常健康人,分离外周血CD19阳性B细胞,以流式细胞仪荧光抗体标记检测其CD154的表达,并体外观察抗CD154抗体对外周血B细胞的增生及IgG分泌的影响。结果(1)活动期SLE外周血B淋巴细胞中CD154阳性率(35±14)%及表达强度(312±108)均显著高于正常健康人,后者分别为(9±7)%、(98±41)(P均<0.001);(2)体外单独培养,活动期SLE外周血B淋巴细胞自身即可异常增生并分泌IgG,[3H]-TdR掺入及体外培养上清液IgG浓度与正常人相比,差异有显著性(P值分别<0.0001和0.001)。抗CD154抗体可显著抑制活动期SLE外周血B淋巴细胞的异常增生及IgG的异常分泌,[3H]-TdR掺入及体外培养上清液IgG浓度与对照抗体组相比,差异有显著性(P值分别为0.01和0.05)。结论CD154在活动期SLE的B淋巴细胞中有异常表达,其异常调控可能是导致分泌自身抗体B细胞克隆增生的主要原因。     

EB病毒与类风湿关节炎的相关性分析

目的:检测EB病毒VCA-IgA抗体在类风湿关节炎(RA)患者外周血中的表达,探讨EB病毒与RA的相关性.方法:分别采用酶联免疫吸附试验(ELISA)法和实时定量PCR方法检测EB病毒VCA-IgA抗体和EB病毒DNA载量.同时分析EB病毒VCA-IgA抗体与RA患者的实验室指标抗CCP抗体、类风湿因子(RF)和血沉(ESR)的相关性.结果:223例SLE患者中,32例为EBV-VCA-IgA抗体阳性,259例健康对照者中16例阳性,KA患者阳性率明显高于对照组(14.35%VS 6.17%;P<0.01).RA患者EB病毒栽量也明显高于对照组.EB病毒VCA-IgA抗体阳性与抗CCP抗体、RF和ESR不相关.结论:EB病毒感染与RA相关.EB病毒VCA-IgA抗体阳性者有较高的DNA载量,RA的发病危险性亦高,EB病毒重新活化与RA活动有关.     

抗中性粒细胞胞浆抗体、抗核抗体联合检测对类风湿关节炎 的诊断价值

目的:探讨抗中性粒细胞胞浆抗体(ANCA)与抗核抗体(ANA)联合检测对类风湿关节炎的临床意义。方法:采用IIF法对82例RA患者(RA组)、74例非RA自身免疫疾病患者(非RA组)和52例健康体检者(正常对照组)的血清ANCA和ANA谱进行了检测分析,并用ELISA法进行抗丝氨酸蛋白酶3(PR3)、抗髓过氧化物酶(MPO)、ANA谱的定量检测。结果:RA组82例患者中,64例ANCA阳性,阳性率为78.08%,其中核周型(PANCA)37例,阳性率为45.1%,胞浆型(CANCA)27例,阳性率为32.9%;非RA组74例患者中有7例ANCA阳性率分别为9.4%;正常对照组50例中没有一例ANCA阳性。利用Elisa法对患者血清进行检测,分别能够特异的检测到PR3、MPO、抗双链DNA抗体(抗ds-DNA抗体)、抗ss-A等抗体、抗SS-A抗体、抗PM-SCL抗体的存在。结论:联合ANCA、ANA检测有助于提高类风湿关节炎的诊断。     

葡萄糖-6-磷酸异构酶抗原对类风湿关节炎的诊断价值

目的:通过比较类风湿关节炎(Rheumatoid arthritis,RA)患者、非RA风湿病患者及健康对照者血清中葡萄糖-6-磷酸异构酶(glucose-6-phosphate isomerase,GPI)抗原的阳性率来探讨GPI对RA的诊断意义,并探讨GPI,抗CCP抗体和RF联合应用对RA的诊断价值.方法:对110例RA患者、223例非RA风湿病患者和55例健康对照者共388份血清标本进行了检测.GPI抗原和抗CCP抗体采用ELISA方法,RF采用免疫比浊法定量检测.结果:RA组、非RA风湿病组和健康对照组血清中的GPI抗原阳性率分别为83.64%,30.04%和20.00%,RA组阳性率显著高于其它组(P＜0.01).GPI抗原对RAt诊断的敏感性和特异性分别为83.64%和71.58%.GPI和抗CCP抗体联合检测的敏感性和特异性分别为90.91%和71.22%,GPI和RF联合检测的敏感性和特异性分别为92.73%和 61.87%,如果三者同时检测,其敏感性和特异性分别为94.55%和60.43%.结论:RA患者的血清GPI阳性率明显高于其它自身免疫性疾病患者和健康对照者.GPI抗原时RA具有诊断价值,联合检测GPI、抗CCP抗体和RF可以提高RA诊断的敏感性.     

无偿献血者ALT异常与戊型肝炎病毒感染的关系

目的 了解无偿献血者ALT异常（按血站标准,以大于25赖氏单位为异常）与戊型肝炎病毒感染的关系。方法 对萧山地区2004年8～11月无偿献血者中,ALT异常的102例血清标本,进行抗-HEV IgM抗体检测;同时对照检测450份ALT正常的无偿献血者血清标本。结果 在102例ALT异常血清中,抗-HEV IgM抗体阳性为6例,阳性率为5.88%,在450份ALT正常血清中,抗-HEV IgM抗体阳性为5例,阳性率为1.11%。结论 在无偿献血者ALT异常血清中,抗-HEV IgM抗体检出比例较高。     

ANCA与SLE临床表现的相关性及其意义

目的:探讨系统性红斑狼疮(Systemic Lupus Erythematosus,SLE)患者抗中性粒细胞胞浆抗体(Anti-neutrophil Cytoplasmic Antibodies,ANCA)与肾炎及其他临床表现和实验室检查的相关性及其意义.方法:采用前瞻性研究收集77例系统性红斑狼疮患者,用间接免疫荧光法(IIF)检测患者血清ANCA、ELISA法检测ANCA抗原,检测其他免疫学指标如抗核抗体、抗dsDNA抗体等.结果:77例SLE患者中ANCA阳性28(36.4%)例,ANCA阳性组浆膜炎、肾损害、神经精神症状、皮肤血管炎、抗dsDNA抗体阳性、抗Sm抗体阳性、补体下降以及血清IgG升高的发生率明显高于阴性组(P＜0.05).52例LN患者中,25例(48.1%)ANCA阳性,其中P-ANCA阳性者22例(88%).3例(12%)为a-ANCA均出现在RPGN,无一例出现c-ANCA.非LN组25例患者中,仅3例(12%)p-ANCA阳性,且均为抗-MPO.正常对照组无一例ANCA阳性.77例SLE患者中,14例(18.2%)为抗-MPO;13例(16.9%)为抗LF,且只见于DPGN、FPGN和RPGN伴有新月体形成者;10例(13%)为抗-CG,但在非狼疮肾炎患者未检测到抗-LF及抗-CG.在各种临床表现中,抗-MPO与肾脏和皮肤表现有关;而抗-LF与肾脏、关节炎及浆膜炎有关;抗-CG可见于各种临床表现.结论:ANCA可作为评价SLE疾病及鉴别血管炎和狼疮肾炎的一个重要指标.     

评价抗SSA、抗SSB 和抗a- 胞衬蛋白抗体在诊断干燥 综合征中的价值

目的：评价SSA、SSB 和胞衬蛋白在诊断干燥综合征(SS)中的价值。方法：用酶联免疫吸附试验（ELISA）检测47 例确诊为SS 患者、20 例其它自身免疫病(类风湿关节炎7 例、SLE6 例、自身免疫性肌炎7 例)和20 例体检健康者血清抗SSA、SSB 和a- 胞衬 蛋白抗体,分析三种自身抗体阳性率。结果：抗SSA抗体、抗SSB 抗体和抗a-胞衬蛋白抗体敏感性分别为76.6%、38.3%、42.6%; 特异性分别为72.5%、95.0%、82.5%;三种抗体联合检测后敏感性为89.4%,特异性50.0%。结论：抗a- 胞衬蛋白抗体与抗SSA、 SSB 抗体联合检测时可提高阳性率,对症状不典型的SS 患者诊断有一定的补充意义。     

No evidence for a putative involvement of platelet-activating factor in systemic lupus erythematosus without active nephritis

BACKGROUND: Platelet-activating factor (PAF) seems to be implicated in systemic lupus erythematosus (SLE) patients with associated renal diseases. AIMS: In this study, we ensured the role of PAF in SLE patients without renal complications. METHODS: Blood PAF and acetylhydrolase activity, plasma soluble phospholipase A(2), and the presence of antibodies against PAF were investigated in 17 SLE patients without active nephritis and in 17 healthy controls. RESULTS: Blood PAF levels were not different (p=0.45) between SLE patients (6.7+/-2.8 pg/ml) and healthy subjects (9.6+/-3.1 pg/ml). Plasma acetylhydrolase activity (the PAF-degrading enzyme) was significantly (p=0.03) elevated in SLE patients (57.8+/-6.4 nmol/min/ml) as compared with controls (37.9+/-2.6 nmol/min/ml). Plasma soluble phospholipase A(2) (the key enzyme for PAF formation) was not different (p=0.6) between SLE patients (59.1+/-5.1 U/ml) and controls (54.7+/-2.4 U/ml). Antibodies against PAF were detected only in 3/17 SLE patients. Flow cytometry analysis did not highlight PAF receptors on circulating leukocytes of SLE patients. CONCLUSION: This clinical study highlights no evidence for a putative important role of PAF in SLE patients without active nephritis.     

抗t-PA抗体水平和血栓的相关性研究

目的:研究自身免疫性疾病病人抗t-PA抗体水平和病人血栓形成之间的关系。方法:用酶联免疫吸附法(ELISA)检测原发性抗磷脂综合症和红斑狼疮患者(32例狼疮样抗凝物阳性,32例狼疮样抗凝物阴性)与40例健康对照的IgG类抗t-pA抗体的水平,用Pearson Chi-Square test的方法分析了病人体内IgG类抗t-PA抗体水平和血栓之间的相关性。结果:本试验研究的病人群体中IgG类抗t-PA抗体阳性的有13(20.3%)个,并且我们的研究表明IgG类抗t-PA抗体阳性和血栓病史显著相关(P=0.04)。结论:原发性抗磷脂综合症和红斑狼疮病人群体中有较高的IgG类抗t-PA抗体水平,它们可能和病人体内血栓的发生有关。     

腺苷脱氨酶及同工酶对自身免疫病诊断和病情监测的作用

摘要 目的：检测腺苷脱氨酶(ADA)及其同工酶在自身免疫病患者血清中的变化,探讨其诊断和病情监测作用。方法：收集70例系统性红斑狼疮（SLE）、114例类风湿性关节炎(RA)、55例强直性脊柱炎(AS)、及其年龄性别对应的健康血清标本。测定血清总ADA（tADA）、ADA1及ADA2活性。ROC曲线分析其诊断价值。结果：与健康对照相比,ADA活性在SLE患者血清中显著升高[tADA：15（12,20）vs 8（7,10）U/L;ADA1：3.5（2,5）vs 3（2,3）U/L;ADA2：11（8,15）vs 6（5,7）U/L;P<0.01）]。与健康对照相比,RA患者血清中tADA和ADA1活性无显著变化(P>0.05),ADA2活性水平升高[8（5.25,10）vs 7（5,9）U/L,P<0.05）];与健康对照相比,AS患者血清中tADA和ADA1活性无显著变化(P>0.05),ADA2活性升高[7（5,9）vs 6（5,7）U/L,P<0.05）]。ROC分析显示tADA及ADA2对SLE具有较好诊断价值（tADA：88.6%特异性、77.1%敏感性;ADA2：92.9%特异性、68.6%敏感性）。ADA活性对RA及AS患者无诊断价值。spearman相关性分析显示,tADA活性与SLE患者疾病活动度有一定正相关性（r=0.303,P=0.011)。结论：血清tADA活性检测可作为SLE辅助诊断和病情监测指标。     

Increased frequency of pre-germinal center B cells and plasma cell precursors in the blood of children with systemic lupus erythematosus

We have analyzed the blood B cell subpopulations of children with systemic lupus erythematosus (SLE) and healthy controls. We found that the normal recirculating mature B cell pool is composed of four subsets: conventional naive and memory B cells, a novel B cell subset with pregerminal center phenotype (IgD(+)CD38(+)centerin(+)), and a plasma cell precursor subset (CD20(-)CD19(+/low)CD27(+/++) CD38(++)). In SLE patients, naive and memory B cells (CD20(+)CD38(-)) are approximately 90% reduced, whereas oligoclonal plasma cell precursors are 3-fold expanded, independently of disease activity and modality of therapy. Pregerminal center cells in SLE are decreased to a lesser extent than conventional B cells, and therefore represent the predominant blood B cell subset in a number of patients. Thus, SLE is associated with major blood B cell subset alterations.     

Monocyte activation by apoptotic cells removal in systemic lupus erythematosus patients

Decreased apoptotic cells (ACs) removal has been described as relevant in systemic lupus erythematosus (SLE) pathogenesis. Binding/phagocytosis of ACs was decreased in SLE patients. Blocking experiments suggested a role for CD36 in ACs clearance in healthy controls, not observed in SLE patients. Binding/phagocytosis of ACs induced the production of IL-6, CXCL8 and CCL22 in patients and controls and IL-1β, TNF-α and CCL3 only in healthy controls. ACs clearance induced an increase in CD80 and a decrease in CD86 expression in healthy controls and atherosclerotic patients. However, SLE patients did not up-regulate CD80 expression. The number and expression of CD36 and CD163 in monocytes was not different between the groups. ACs removal induced a down-regulation of CD36 expression in adherent HLA-DR⁺ cells in SLE patients but not healthy controls. The decreased binding/phagocytosis of ACs observed in SLE patients, induces a distinct immune response compared with healthy controls.     

Identification of three new autoantibodies associated with systemic lupus erythematosus using two proteomic approaches

Our objective was to identify new serum autoantibodies associated with systemic lupus erythematosus (SLE), focusing on those found in patients with central nervous system (CNS) syndromes. Autoantigens in human brain proteins were screened by multiple proteomic analyses: two-dimensional polyacrylamide gel electrophoresis/Western blots followed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis and immunoprecipitation followed by liquid chromatography-tandem mass spectrometry shotgun analysis. The presence of serum IgG autoantibodies against 11 selected recombinant antigens was assessed by Western blot and enzyme-linked immunosorbent assay (ELISA) in the sera of 106 SLE patients and 100 normal healthy controls. The O.D. values in sera from SLE patients were significantly higher than those of controls for the antigens crystallin αB (p = 0.0002), esterase D (p = 0.0002), APEX nuclease 1 (p < 0.0001), ribosomal protein P0 (p < 0.0001), and PA28γ (p = 0.0005); the first three are newly reported. The anti-esterase D antibody levels were significantly higher in the CNS group than in the non-CNS group (p = 0.016). Moreover, when the SLE patients were categorized using CNS manifestations indicating neurologic or psychiatric disorders, the anti-APEX nuclease 1 antibody levels were significantly elevated in SLE patients with psychiatric disorders (p = 0.037). In conclusion, the association of SLE with several new and previously reported autoantibodies has been demonstrated. Statistically significant associations between anti-esterase D antibodies and CNS syndromes as well as between anti-APEX nuclease 1 antibodies and psychiatric disorders in SLE were also demonstrated. The combined immunoproteomic approaches used in this study are reliable and effective methods for identifying SLE autoantigens.     

趋化因子CXCL14在SLE患者外周血单个核细胞中的表达及启动子甲基化分析

目的：分析趋化因子CXCL14在系统性红斑狼疮（SLE）患者外周血单个核细胞（PBMC）中的表达及其启动子甲基化特征。方法：收集28例SLE患者和20名健康人外周血单个核细胞（PBMC）标本,抽提细胞中RNA,逆转录后,以GAPDH为内参,通过定量PCR检测PBMC中CXCL14的表达,统计分析CXCL14表达水平与SLE各种临床资料的相关性,探讨PBMC中CXCL14表达与SLE的关系,通过重亚硫酸盐修饰的全基因组DNA用以BSP测序来明确不同标本中CXCL14启动子中甲基化位点的甲基化率。结果：CXCL14在SLE患者和正常人PBMC中的表达量存在显著差异（P < 0.05）。与健康人PBMC中CXCL14的含量相比较,CXCL14在SLE患者PBMC中表达量显著降低。与进一步CXCL14表达水平与SLE各种临床资料的相关性分析显示,CXCL14表达水平与SSB抗体（干燥综合征B抗体）、蛋白尿及血小板计数相关。与SSB抗体阴性SLE患者比较,SSB抗体阳性患者CXCL14表达水平更低（P <0.05）;与蛋白尿阴性SLE患者相比,蛋白尿阳性患者CXCL14表达水平更低（P < 0.05）;而血小板升高患者的CX-CL14表达水平更高（P < 0.05）。CXCL14表达水平与SLE活动、肾损害指标、抗ds-DNA、C反应蛋白（CRP）、补体C3水平等指标未见显著相关性。CXCL14启动子区甲基化分析显示,SLE患者CpG岛甲基化明显高于正常对照。结论：PBMC中低表达的CXCL14与SLE发生发展相关,其启动子区CpG岛过度甲基化是SLE患者CXCL14低表达的重要机制。     

Th 细胞因子IL-17、IFN-γ、IL-4 在狼疮性肾炎中的表达及意义

目的:探讨T辅助细胞(Th)相关细胞因子在狼疮性肾炎发病中的免疫机制作用。方法:64例系统性红斑狼疮患者和28例健康体检者作为对照,采用酶联免疫吸附测定法(ELISA法)检测所有受试者血清IL-17、IFN-γ、IL-4水平,并对其与SLEDAI、SDI、24小时尿蛋白量相关性进行研究。结果:狼疮性肾炎组血清IL-17水平显著高于狼疮无肾炎组和健康对照组(P<0.001),狼疮性肾炎组血清IFN-γ水平显著高于狼疮无肾炎组(P<0.05)和健康对照组(P<0.01),血清IL-4水平在狼疮性肾炎组、狼疮无肾炎组均显著高于健康对照组(P<0.01)。狼疮性肾炎组IFN-γ/IL-4比值显著高于狼疮无肾炎组(P<0.01)和健康对照组(P<0.05);狼疮无肾炎组IFN-γ/IL-4比值显著低于健康对照组(P<0.01)。SLE患者血清IFN-γ表达水平与SLEDAI积分呈正相关(r=0.402,P<0.05),血清IL-17、IL-4表达水平与SLEDAI、SDI、抗ds-DNA抗体、C3、24小时尿蛋白量均无相关性。结论:狼疮性肾炎患者外周血中IL-17、IFN-γ、IL-4等促炎细胞因子均有不同程度升高促起炎症发生及组织损伤,参与了狼疮性肾炎的免疫发病过程。     

Detecting clinical activity in systemic lupus erythematosus with an archaeal poly(ADP-ribose) polymerase-like thermozyme: a pivotal study

The clinical usefulness of an immunotest was evaluated by using purified poly(adenosine diphosphate (ADP)-ribose) polymerase from Sulfolobus solfataricus (PARPSso) as an antigen to detect the presence of abnormal anti-PARP antibodies in the sera of patients with systemic lupus erythematosus (SLE) at different clinical stages. Sera from 44 patients with SLE, subgrouped on the basis of disease activity (16 with inactive disease, 28 with active disease) were analysed with a new immunotest to detect anti-PARP antibodies, and with an immunofluorescent (IIF) assay for antinuclear antibodies (ANA) detection. ANA detection by IIF revealed that sera of healthy subjects were negative, whereas sera from patients with SLE were positive in all cases (13 positive at 1:80, 15 at 1:160, 15 at 1:320, 1 at 1:640, v/v). Anti-PARP activity was higher in ANA-positive patients than in controls (p?=?0.005). Within the group of SLE sera, disease and anti-PARP activity was increased more significantly in patients with active than in those with inactive disease (p?p?=?0.001, respectively). Correlation between anti-PARP and disease activity in SLE patients was statistically significant (p?Sso seems to be suitable for detecting anti-PARP antibodies and could play a role as a serological marker of disease activity in patients with SLE.     

Constitutive phosphorylation of interferon receptor a-associated signaling proteins in systemic lupus erythematosus

Background

Overexpression of type I interferon (IFN-I)-induced genes is a common feature of systemic lupus erythematosus (SLE) and its experimental models, but the participation of endogenous overproduction of IFN-I on it is not clear. To explore the possibility that abnormally increased IFN-I receptor (IFNAR) signaling could participate in IFN-I-induced gene overexpression of SLE, we examined the phosphorylation status of the IFNAR-associated signaling partners Jak1 and STAT2, and its relation with expression of its physiologic inhibitor SOCS1 and with plasma levels of IFNα and IFN-like activity.

Methodology/Principal Findings

Peripheral blood mononuclear cells (PBMC) from SLE patients with or without disease activity and healthy controls cultured in the presence or in the absence of IFNβ were examined by immunoprecipitation and/or western blotting for expression of the two IFNAR chains, Jak1, Tyk2, and STAT2 and their phosphorylated forms. In SLE but not in healthy control PBMC, Jak1 and STAT2 were constitutively phosphorylated, even in the absence of disease activity (basal pJak1: controls vs. active SLE p<0.0001 and controls vs. inactive SLE p = 0.0006; basal pSTAT2: controls vs. active and inactive SLE p<0.0001). Although SOCS1 protein was slightly but significantly decreased in SLE in the absence or in the presence of IFNβ (p = 0.0096 to p<0.0001), in SOCS1 mRNA levels were markedly decreased (p = 0.036 to p<0.0001). IFNβ induced higher levels of the IFN-I-dependent MxA protein mRNA in SLE than in healthy controls, whereas the opposite was observed for SOCS1. Although there was no relation to increased serum IFNα, active SLE plasma could induce expression of IFN-dependent genes by normal PBMC.

Conclusions/Significance

These findings suggest that in some SLE patients IFN-I dependent gene expression could be the result of a low IFNAR signaling threshold.