重症肌无力患者汉密尔顿抑郁量表评分分析

目的探讨重症肌无力(myasthenia gravis,MG)患者汉密尔顿抑郁量表(Hamilton depression rating scale,HDRS)评分情况及其影响因素分析。方法横断面研究2013-07—2015-03作者医院就诊的188例MG患者的临床资料和HDRS评分情况,并根据HDRS评分将其分为抑郁组和非抑郁组,分析两组MG患者的临床特点及其与HDRS评分间的关系。结果所纳入MG患者男女比例为1.02∶1,眼肌型重症肌无力(ocular myasthenia gravis,OMG)和全身型重症肌无力(generalized myasthenia gravis,GMG)的比例为1.2∶1,以OMG起病和以GMG起病患者的比例为6.2∶1,病程中位数为2年,四分位数间距为1.8年,平均量化重症肌无力评分(quantitative myasthenia gravis,QMG)为(6.7±2.3)分,平均HDRS评分为(8.7±3.4)分,并发抑郁者65例,未并发抑郁者123例。影响HDRS评分和抑郁发生的相关因素包括性别(P0.01)、MG类型(P0.01)、QMG得分(P0.01)和美国重症肌无力协会(myasthenia gravis foundation of America,MGFA)分型(P0.01)、有无甲状腺功能亢进(P0.05)。结论影响MG患者HDRS评分和抑郁发生的相关因素包括性别、MG类型、QMG评分和MGFA分型、有无甲状腺功能亢进,充分认识其抑郁发生情况有利于更好地治疗MG。     

眼肌型及全身型重症肌无力患者外周血T淋巴细胞Fas的表达

目的 探讨Fas介导的细胞凋亡与眼肌型(ocular myasthenia gravis,OMG)及全身型重症肌无力(generalized myasthenia gravis,GMG)发病的关系.方法 采用流式细胞技术检测4例OMG、13例GMG患者及13例健康对照组外周血淋巴细胞中CD4、CD8及Fas的表达.结果 OMG、GMG组与对照组外周血T淋巴细胞表面CD4、CD8分子表达的差异无统计学意义(P>0.05).GMG组与对照组外周血T淋巴细胞中Fas+细胞比例的差异有统计学意义(41.72%±8.73%、31.22%±13.00%,P:0.017).GMG组与对照组Fas表达增高者比例的差异有统计学意义(61.5%、15,4%,P=0.041).Fas表达增高的GMG患者病情较重.病程较长.胸腺瘤发生率较高.OMG与GMG组外周血T淋巴细胞中Fa8+、CD4+Fas+、CD8+Fas+细胞比例差异无统计学意义(P>0.05).结论 GMG患者外周血T淋巴细胞中Fas的表达升高,OMG与GMG患者外周血T淋巴细胞中Fas的表达无显著差异,二者可能同属一种系统性疾病.     

重症肌无力患者外周血Th17细胞及其相关细胞因子表达研究

目的研究重症肌无力患者外周血辅助性T细胞17(Th17)及其相关细胞因子水平,探讨其与血清抗乙酰胆碱受体(AChR)抗体水平的相关性。方法纳入2016年9月至2017年12月共30例初诊重症肌无力患者,眼肌型(OMG) 16例、全身型(GMG) 14例。流式细胞术检测外周血单个核细胞Th17细胞比例,实时定量聚合酶链反应检测Th17细胞标志性细胞因子白细胞介素-17A(IL-17A)及其相关转录因子维A酸相关孤儿受体γ(RORγ)mRNA水平,酶联免疫吸附试验检测血浆IL-17A、IL-6、IL-23和抗AChR抗体水平。结果与正常对照组相比,GMG组和OMG组外周血Th17细胞比例(t=-3.312,P=0.002;t=-2.286,P=0.030)及其相关转录因子RORγmRNA表达水平(f=4.408,P=0.001;t=1.991,P=0.049),以及IL-17A水平(t=-4.282,P=0.004;t=-2.788,P=0.007)均高于正常对照组;GMG组IL-23水平亦高于正常对照组(t=-2.267,P=0.031)。重症肌无力患者外周血Th17细胞比例及血浆IL-17A水平与血清抗AChR抗体水平呈正相关(r=0.851,P=0.012;r=0.743,P=0.025)。结论重症肌无力患者外周血Th17细胞数目增加、血浆IL-17A表达水平升高,可能是导致重症肌无力发生与发展的重要原因,二者之间关系尚待进一步研究加以证实。     

microRNA-181c在重症肌无力患者外周血单个核细胞中的表达及其意义

目的探讨microRNA-181c(miR-181c)在重症肌无力(myasthenia gravis,MG)患者中的表达水平及其临床意义。方法收集2015年6月-2017年6月收治的22例MG患者和20例健康人的外周静脉血样,提取外周血单个核细胞(peripheral blood mononuclear cell,PBMC)中总RNA,采用实时定量PCR(quantitative real-time PCR,qRT-PCR)技术检测PBMC中miR-181c的相对表达水平,并分析miR-181c表达水平与患者的MG定量评分体系(quantitative myasthenia gravis score,QMG)的相关性。结果 MG患者PBMC中miR-181c的相对表达水平(0.303±0.150)较对照组(1.000±0.262)显著降低(P0.01),其中全身型患者(0.182±0.056)低于眼肌型患者(0.404±0.126)(P0.05),同时miR-181c表达水平与QMG呈负相关(R2=-0.359,P0.05)。结论 MG患者PBMC中miR-181c表达水平的降低可能与病情严重程度有关。     

重症肌无力患者外周血AIRE、Tfh细胞和Tfr细胞与病情严重性相关分析

目的探讨自身免疫性调节因子(AIRE)、滤泡辅助性T(Tfh)细胞和滤泡调节性T(Tfr)细胞与重症肌无力(MG)患者病情严重程度的相关性。方法收集2015-12—2016-4第四军医大学唐都医院收治的MG患者22例,根据临床表现分为全身型MG(GMG)和眼肌型MG(OMG);同期选取健康体检中心查体者10名作为健康对照。收集MG患者详细临床资料,包括美国MG协会(MGFA)分型及定量MG(QMG)评分。通过流式细胞术分析AIRE阳性细胞比例及Tfh/Tfr比值。结果 (1)AIRE表达在各组间比较差异具有统计学意义(P0.01)。GMG组和OMG组AIRE表达均较对照组降低(P0.01,P0.05),而GMG组与OMG组间比较差异无统计学意义(P0.05)。(2)Tfh/Tfr比值在各组间比较差异具有统计学意义(P0.01)。GMG组和OMG组Tfh/Tfr比值均高于对照组(P0.01,P0.05),且GMG组高于OMG组(P0.05)。(3)MG患者AIRE表达与MGFA分型及QMG评分呈负相关(r=-0.517,P0.05;r=-0.616,P0.01),Tfh/Tfr比值与MGFA分型和QMG评分呈正相关(r=0.761,r=0.581,均P0.01)。结论 AIRE、Tfh/Tfr比值与MG的病情严重程度有一定的相关性,并可能参与了MG的发病。     

眼肌型重症肌无力研究进展及临床问题

在重症肌无力(MG)患者中眼肌型重症肌无力(ocular myasthenia gravis,OMG)是最常见的临床类型,在我国OMG发病率较高。OMG患者表现的眼外肌无力(如上睑下垂)可以直观地显示MG患者的表征特点,以及表现为晨轻暮重或活动     

眼肌型和全身型重症肌无力的差异

重症肌无力(myasthenia gravis,MG)是由乙酰胆碱受体抗体(acetylcholine receptor antibody,AChRAb)介导的、细胞免疫依赖的、补体参与的自身免疫性疾病,其主要临床症状为横纹肌收缩无力,多数患者起病表现为眼肌型MG(ocular MG,OMG),以后逐渐进展为全身型MG(generalizedMG,GMG),严重者累及呼吸肌,发生肌无力危象而死亡[1]。     

重症肌无力患者外周血Th17和调节性T细胞分析

目的 观察重症肌无力(myasthenia gravis,MG)患者Th17细胞和调节性T细胞的水平,并研究甲强龙冲击治疗对其影响.方法 应用四色流式细胞仪检测66例MG患者及35名健康对照者外周血Th17细胞和CD4+CD25highT细胞百分率;分析其中18例患者外周血Th17细胞与美国MG协会(MGFA)评分相关性;观察8例MG患者甲强龙冲击治疗2周后上述细胞的变化.结果 MG患者与健康对照者外周血Th17细胞百分率分别为2.61%±0.28%与0.94%±0.12%(Z=4.059,P=0.0001);甲强龙治疗前后8例MG患者Th17细胞百分率分别为4.72%±1.21%与1.81%±0.69%,差异有统计学意义(Z=1.995,P=0.0460);患者外周血Th17细胞水平与MGFA评分呈正相关(r=0.5359,P=0.0219).结论 MG患者外周血中Th17细胞升高,甲强龙冲击治疗可降低其水平,这可能是改善MG患者病情的有效机制.     

重症肌无力患者Foxp3~+CD4~+CD25~+调节性T细胞与AChRAb、Titin-Ab的相关研究

目的探讨重症肌无力(myasthenia gravis,MG)患者Foxp3~+CD4~+CD25~+调节性T细胞(Foxp3~+CD4~+CD25~+Treg)与乙酰胆碱受体抗体(AChRAb)及连接素抗体(Titin-Ab)之间的关系,进一步揭示MG的发病机制。方法采用酶联免疫吸附试验(ELISA)检测22例MG患者以及20名健康对照者血清AChRAb和Titin-Ab水平;采用流式细胞术(FCM)检测两组外周血中CD4~+CD25~+Treg的比例及其表达Foxp3的比例。结果 MG患者外周血CD4~+CD25~+Treg比例[(2.9±0.52)%]与健康对照组[(3.12±0.51)%]比较无统计学差异(P0.05);CD4~+CD25~+Treg细胞Foxp3表达比例为(37.24±9.57)%,低于健康对照组[(58.60±4.91)%](P0.01)。MG组CD4~+CD25~+Treg表达Foxp3比例与AChRAb、Titin-Ab水平[分别为(0.232±0.060)和(0.170±0.035)pg/mL]均呈负相关(r=-0.449,P0.05;r=-0.691,P0.01)。结论 Foxp3~+CD4~+CD25~+Treg细胞数目减少导致机体免疫功能缺陷是MG发病的重要环节。     

小儿眼型重症肌无力向全身型转化的临床特点

目的 研究小儿眼型重症肌无力(ocular myasthenia gravis,OMG)向全身型重症肌无力(generalized myasthenia gravis,GMG)的转型率、转型时间及使用泼尼松对转型的影响.方法 回顾性分析1977至2005年青岛大学医学院附属医院诊治的978例小儿OMG转变为GMG的转型率、转型时间以及泼尼松对转型的影响,并与同期诊治的1359例成人OMG患者进行对比分析.结果 小儿OMG转化为GMG的转型率为13.0%(127/978),而成人OMG的转型率为67.2%(913/1359),两组差异有统计学意义(χ2=674.17,P<0.01).OMG的转型时间大多在发病后的2年内,小儿OMG(58.3%,74/127)与成人OMG(83.6%,763/913)在发病后2年内转型的比率差异有统计学意义(χ2=45.39,P<0.01).使用泼尼松的456例小儿OMG患者中仅有5例(1.1%)转为GMG,而从未使用过泼尼松的522例小儿OMG患者中有122例(23.4%)变为GMG,差异有统计学意义(χ2=104.9,P<0.01).结论 小儿OMG转型率与成人OMG相比显著减少;转型的时间大多在发病后头2年内;泼尼松确实能减少小儿OMG向GMG转化的机会.     

放射免疫法定量检测乙酰胆碱受体抗体与重症肌无力患者临床特征的相关性

目的探讨乙酰胆碱受体抗体(AChR-Ab)与重症肌无力(MG)临床特征的相关性。方法采用放射免疫法检测115例MG患者及92例对照组(非MG神经系统疾病患者42例,健康体检者50名)血清AChRAb浓度,应用临床绝对评分记录MG患者病情严重程度。分析各组血清AChR-Ab浓度的差异,以及AChR-Ab浓度与MG患者临床特征的相关性。采用ROC工作特征曲线探讨AChR-Ab诊断MG的敏感度和特异度。结果MG患者血清AChR-Ab浓度中位数(四分位数间距,下同)为3.45(39.38)nmol/L,较非MG神经系统疾病患者[0(0)nmol/L]和健康体检者[0(0)nmol/L]增高(P0.01)。全身型MG(GMG)患者AChR-Ab浓度[25.45(46.14)nmol/L]较眼肌型MG(OMG)患者[0.58(3.56)nmol/L]增高(P0.01)。用ROC曲线法分析显示,以血清AChR-Ab浓度≥0.50nmol/L作为诊断MG界值时灵敏度为72.17%,特异度为100%,曲线下面积(AUC)=0.895(95%CI:0.849~0.941)。AChR-Ab浓度与发病年龄、病程及改良Osserman分型呈正相关(r=0.220,P0.05;r=0.184,P0.05;r=0.382,P0.01),但相关性较弱(均r0.5),与临床绝对记分无相关性(r=0.147,P0.05)。结论用放射免疫法检测血清AChR-Ab浓度诊断MG的灵敏度和特异度均高,有助于减少MG的漏诊率及误诊率,值得临床推广。     

癫痫患儿外周血CD19+B、 CD20+B淋巴细胞和自然杀伤细胞的检测及意义

目的探讨儿童癫痫患者外周血CD 19+13、CD20+B淋巴细胞和自然杀伤(NK)细胞的表达及其意义。方法选择中山大学孙逸仙纪念医院自2008年1月至2010年12月收治的癫痫患儿458例为病例组,另设同期该院52例健康对照者为对照组。应用流式细胞仪对2组成员外周血CD19+B细胞、CD20+B细胞和NK细胞的表达进行检测及比较,同时分析92例应用静脉注射免疫球蛋白(IVIG)治疗的癫痫患儿治疗前后细胞表达的改变。 结果癫痫患儿CD19+B细胞和CD20+B细胞比例分别为(22.35％±6.54％)、(21.50％±8.41％),明显高于正常对照组(16.86％±4.02％)、(16.13％±4.19％),差异有统计学意义(P≤0.05); NK细胞比例为(9.11％±4.90％),明显低于正常对照组(14.72％±4.15％),差异有统计学意义(P≤0.05)。IVIG治疗6个月后癫痫患儿CD19+B细胞和CD20+B细胞比例分别为(18.26％±5.03％)、(16.74％±5.12％),较治疗前(22.74％±6.25％)、(21.61％±8.03％)明显降低,差异有统计学意义(P＜0.05);而NK细胞为(14.65％±4.58％),较治疗前(9.07％±4.76％)明显升高,差异亦有统计学意义(P＜0.05)。92例IVIG治疗患儿中,22例无效,70例有效,有效与无效患儿外周血CD19+B细胞和CD20+B细胞比例治疗前后差值差异具有统计学意义(P＜0.05),但外周血NK细胞比例治疗前后差值差异无统计学意义（P＞0.05）。 结论癫痫患儿存在B淋巴细胞和NK细胞功能异常,IVIG治疗能改善癫痫患儿的免疫功能紊乱;外周血CD19+B细胞、CD20+B细胞可做为癫痫IVIG治疗疗效的监测指标。     

Expression of Immune Molecules CD25 and CXCL13 Correlated with Clinical Severity of Myasthenia Gravis

Differential expressions of immune molecules have been shown in the thymi with pathological results, including myasthenia gravis (MG). CD25 is an activation marker expressed on T cells. CXCL13 mediates the homing and motility of B cells in secondary lymphoid tissues. Herein, we investigated the expressions of CD25 and CXCL13 in the thymi of thymic hyperplasia patients with MG or with non-MG. A total of 34 thymic hyperplasia patients with MG (20 generalized MG (GMG) and 14 ocular MG (OMG) and six thymic hyperplasia patients without MG were enrolled and analyzed using immunohistochemical staining and real-time polymerase chain reaction for CD25 and CXCL13. Our study demonstrated a higher expression of both CD25 and CXCL13 in hyperplastic thymi with OMG or GMG compared to those with non-MG. According to the immunohistochemical results, we observed that CD25 expression was significantly lower in atrophic thymi and non-MG hyperplastic thymi, compared with that in infant thymi (P?=?0.002 and 0.005, respectively). In contrast to CD25 expression, we did not observe differential expression of CXCL13 among three control groups. And a similar CD25 mRNA expression was found in real-time polymerase chain reaction (PCR) results. We observed that both hyperplastic thymi with OMG or GMG expressed significantly higher levels of CD25 than those with non-MG (P?=?0.007 and 0.001, respectively). And an increase of CD25 expression was observed in hyperplastic thymi with GMG compared to those with OMG (P?=?0.030). Similarly, CXCL13 expression was significantly higher in hyperplastic thymi with GMG or with OMG than those with non-MG (P?=?0.001 and 0.050, respectively). No significant CXCL13 expression difference was found between hyperplastic thymi with GMG and those with OMG (P?>?0.05). The real-time PCR results showed a similar tendency of CD25 mRNA expression among the thymi of non-MG, OMG, and GMG patients, but the difference did not reach significance (P?>?0.05). An obvious increased expression of CXCL13 was found in hyperplastic thymi with GMG patients, compared to those with non-MG and OMG patients (P?=?0.003 and 0.071, respectively). There was no difference found between hyperplastic thymi with non-MG and with OMG. Regression analysis showed a positive correlation between thymic CD25 level and MG symptom severity (F?=?28.240; P?=?0.000, r?=?0.523). Similarly, a positive correlation was found between thymic CXCL13 expression and MG disease severity (F?=?36.093; P?=?0.000, r?=?0.671). Taken together, our findings suggest CD25 and CXCL13 participate in the pathogenesis of MG and may influence the clinical symptoms of MG.     

Ocular myasthenia gravis: predictive value of single-fiber electromyography.

Extraocular muscle weakness is the most common presenting sign of myasthenia gravis (MG). More than half of patients presenting with symptoms isolated to these muscles (OMG) develop generalized myasthenia gravis (GMG) over the course of their illness. No clinical, laboratory, or electrophysiological features are recognized that identify these high-risk patients. We have therefore assessed the ability of single-fiber electromyography (SFEMG) to predict the development of GMG in patients presenting with OMG. Thirty-nine consecutive patients presenting with OMG underwent SFEMG of the extensor digitorum communis muscle as well as a battery of other laboratory and imaging studies at the time of diagnosis. All patients were followed prospectively for a minimum of 24 months or until they developed GMG. Two patients were excluded, leaving 37 for assessment. Twenty remained with pure OMG for the entire follow-up period (mean, 55 months). Twenty-six of the 37 had abnormal SFEMG studies at presentation. Eleven of these remained with OMG and 15 developed GMG. Fifty-eight percent of patients with an abnormal SFEMG developed GMG, whereas 82% of those with a normal study remained with OMG. Thus, a normal SFEMG was associated with MG remaining restricted to the extraocular muscles. (P = 0.036, Fisher's exact test), but an abnormal SFEMG was not predictive of subsequent development of GMG.     

MG患者外周血Th17细胞与AChR抗体产生的关系研究

目的探讨重症肌无力(MG)患者外周血中Th17细胞及相关细胞因子白细胞介素17(IL-17)在MG发病中的作用。方法收集40例MG患者和10名健康人(对照组)外周血标本,采用流式细胞术检测外周血单个核细胞(PBMCs)中Th17细胞比例,反转录酶-聚合酶链锁反应(RT-PCR)检测PBMCs中维甲酸受体相关孤儿受体γt(RORγt)mRNA水平,ELISA检测血清中IL-17水平,放射免疫沉淀法检测血清中抗乙酰胆碱受体抗体(AChR-Ab)滴度;分离PBMCs中CD4~+T细胞和CD19~+B细胞与金黄色葡萄球菌肠毒素B(SEB)进行共培养,培养系统中加入人IL-17和(或)IL-21中和抗体,放射免疫测定法检测培养液中AChR-Ab滴度。采用MG评分(quantitative MG scoring system,QMGs)对MG的严重程度进行评估,并对MG患者的Th17细胞比例、RORγt mRNA和IL-17水平与病情QMGs的相关性,以及MG患者抗AChR-Ab滴度与PBMCs中Th17细胞比例的相关性进行分析。结果 MG患者PBMCs中Th17细胞比例[1.11%(0.90%,1.34%)]高于健康对照组Th17细胞比例[0.26%(0.08%,0.36%)](z=5.494,P0.001),且与疾病严重程度呈正相关(r=0.4394,P=0.0046);血清中IL-17水平和PBMCs中RORγt mRNA相对表达[分别71.46(53.91,104.76)pg/mL、2.63(1.94,3.12)]均较健康对照组[分别18.82(12.73,29.80)pg/mL、1.13(0.98,1.28)]显著增高(均P0.001);MG患者血清中抗AChR-Ab滴度[2.34(1.19,3.60)nmol/L]较健康对照组[-0.08(-0.24,-0.03)nmol/L]显著增高(z=4.662,P0.001),且与Th17细胞比例呈正相关(r=0.7066,P=0.0001)。MG患者外周血T、B细胞与SEB共培养后抗AChR-Ab水平高于未加入SEB时及健康对照(均P0.01);加入抗人IL-21或IL-17中和抗体后,两者AChR-Ab滴度与未加入抗体时AChR-Ab滴度比较均降低(均P0.05),且均仍高于MG患者未加入SEB时及健康对照(P0.01);在培养上清中同时加入抗人IL-21和IL-17中和抗体时AChR-Ab滴度明显低于加入单种抗体时,而与未加入SEB时及健康对照差异无统计学意义(均P0.05)。结论 MG患者外周血中Th17细胞可能通过IL-17促进AChR-Ab产生,参与疾病的病理过程。     

阿尔茨海默病患者外周血单个核细胞Toll样受体4和9的表达水平

目的 分析AD患者外周血单个核细胞Toll样受体(TLR)4和9的改变,寻找取材容易、特异性高的生物学标志物.方法 纳入72例AD患者,60例年龄、性别匹配的健康状况良好的体检者作为对照组.收集相关临床资料,采集外周血液,分离单个核细胞,采用流式细胞术检测TLR4和TLR9的蛋白表达,采用Real-time PCR检测其mRNA的表达.结果 Real-time PCR结果显示,与对照组相比,AD组TLR4的mRNA表达明显升高(1.43±0.27),而TLR9的mRNA表达明显降低(0.65±0.11),两组比较差异均有统计学意义(P＜0.05).流式细胞结果显示,AD组TLR4的蛋白表达明显升高[(31.5±15.1)％比(10.2±7.5)％],TLR9表达明显降低(17.3±13.2)％比(43.7±20.6)],差异均有统计学意义(P＜0.01).结论 外周单个核细胞参与AD的炎性反应,其TLR4和TLR9的表达改变,有可能作为AD诊断的生物学标准物,为AD的诊断提供新的思路.     

T cell reactivity to P0, P2, PMP-22, and myelin basic protein in patients with Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Objectives: It has been suggested that autoimmunity to peripheral myelin proteins is involved in the pathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). We aimed to compare reactivity of peripheral blood mononuclear cells (PBMC) to antigens of peripheral myelin proteins in patients with GBS and patients with CIDP with that of healthy controls and patients with other non-immune mediated neuropathies (ON). Methods: We prepared PBMC from blood from 83 healthy controls and from 64 patients with GBS, 54 with CIDP, and 62 with ON. PBMC were tested in antigen specific proliferation assays against peptides from myelin proteins P0, P2, PMP22, and myelin basic protein (MBP), which is identical to myelin P1, and against whole human MBP. Interferon-gamma (IFN-γ) and interleukin (IL)-5 enzyme linked immunospot (ELISPOT) assays were also performed in some subjects to assess spontaneous and peripheral myelin antigen specific PBMC cytokine secretion. Results: Antigen specific PBMC proliferation assays showed no significant elevation of peptide specific T cell responsiveness in patients with GBS or CIDP compared with healthy controls or patients with ON. Levels of spontaneous ELISPOT IFN-γ secretion were increased in patients with GBS and significantly increased in those with CIDP compared with healthy controls and patients with ON. No convincing differences in antigen specific ELISPOT IFN-γ secretion levels to individual peptides were detectable in patients with GBS. The proportion of patients with CIDP with an increased number of PBMC producing IFN-γ in response to peptide PMP-22_51–64 was significantly increased compared with healthy controls and patients with ON. No significant differences in antigen specific ELISPOT IL-5 secretion levels were detectable in patients with GBS or CIDP compared with controls, but levels of spontaneous IL-5 secretion were significantly higher in patients with CIDP than in healthy controls or patients with ON. Conclusions: Although the lack of significantly increased antigen specific PBMC proliferation in GBS and CIDP does not support a role for T cells, the more sensitive ELISPOT technique detected increased numbers of PBMC secreting IFN-γ spontaneously in 25% of patients with GBS, providing further evidence for a role of T cells in the immunopathology of GBS. Increased numbers of spontaneous IFN-γ and IL-5 secreting cells, and increased IFN-γ secretion in response to PMP-22_51–64, in patients with CIDP provide further evidence for a role of myelin specific T cells in CIDP.