中间丝聚合蛋白在特应性皮炎患者皮损中的表达

目的：探讨中间丝聚合蛋白（Filaggrin,FLG）在特应性皮炎（Atopic dermatitis,AD）患者皮损的表达及其临床意义。方法：采用sP免疫组化方法检测16例AD患者皮损及14例对照组皮肤组织内FLG的表达,用图像分析软件Image-ProPlus（IPP）判定FLG在AD患者皮损及健康者皮肤组织中阳性染色面积百分比。结果：FLG在AD患者皮损及健康者皮肤角质层及颗粒层均有表达,胞质染色多见;阳性染色面积百分比分别为（18．92±4．40）％及（23．00±2．28）％;FLG在AD患者皮损阳性染色面积明显低于健康人皮肤（t=－3．11,P=0．004）。结论：FLG在AD患者皮损中表达降低,可能是导致AD患者皮肤屏障功能障碍的原因。     

特应性皮炎与丝聚蛋白研究进展

丝聚蛋白(FLG)基因的失功能突变可使表皮FLG含量减少或缺失,进而引起表皮屏障功能发生改变,增加特应性皮炎(AD)的患病风险。本文对FLG在表皮屏障形成中的作用、FLG基因结构、FLG基因在AD患者中的突变情况及FLG基因突变与AD临床表型的相关性进行综述。     

FLG基因SNPs与延边朝鲜族特应性皮炎的相关性

目的探讨丝聚蛋白(FLG)基因单核苷酸多态性(SNPs)与延边地区朝鲜族特应性皮炎(AD)的关系。方法选择70例AD患者和90例正常对照人群作为研究对象,使用PCR法,分析FLG基因2个SNPs位点(rs11584340及rs3126085)的基因型与等位基因情况,探讨AD组及对照组等位基因、基因型频率分布情况。结果 FLG基因2个SNPs rs11584340(G)和rs3126085(G)等位基因频率、基因型频率在AD组、对照组之间均符合Hardy-Weinberg平衡定律(P0.05);在延边朝鲜族人群AD组与对照组之间rs11584340和rs3126085位点的等位基因频率、基因型频率差异无统计学意义(P0.05);rs11584340与rs3126085为强连锁不平衡(D'=1.00,r~2=0.84);延边地区朝鲜族FLG基因2个SNPs的等位基因频率与Hap Map数据库(ss41111533,ss17361789)比较均存在差异,rs11584340-G等位基因频率显著低于非洲人(YRI)和欧洲人(CEU)(P0.01);rs3126085-G等位基因频率显著低于CEU(P0.01)。结论延边朝鲜族rs11584340和rs3126085为强连锁不平衡;FLG基因SNP存在种族差异和民族差异;FLG基因rs11584340和rs3126085多态可能与中国延边地区朝鲜族AD易感性不相关。     

CD40基因多态性及血清水平与系统性红斑狼疮发病机制的相关研究

目的 探讨CD40基因单核苷酸多态性（SNP）及其单倍型与SLE易感性的相关性,分析CD40基因型及血清水平与系统性红斑狼疮（SLE）的相关性。 方法 单碱基延伸的PCR技术（PCR-SBE）和DNA测序法分析205例SLE患者和220例健康对照CD40基因rs1883832 C/T、 rs13040307 C/T、rs752118 C/T 和rs3765459 G/A的多态性,同时用ELISA检测血清CD40水平。 结果 与健康对照组相比,SLE组血清CD40水平显著增高（P < 0.05）。SLE组与健康对照组CD40基因rs1883832 C/T位点基因型和等位基因频率比较,差异有统计学意义（P < 0.01）。等位基因频率的相对风险分析后发现,携带有rs1883832 T等位基因的受试者患有SLE的风险是rs1883832 C等位基因的1.517倍（OR = 1.517,95% CI 1.157 ~ 1.990,P = 0.003）;携带rs1883832 T等位基因的SLE患者血清CD40水平与不携带者相比,结果显著增高（P < 0.01）。通过联合基因型分析发现,SLE组中携带单倍型TCCA的患者较健康对照组显著增加了发病的风险（OR = 2.322,95% CI 1.181 ~ 4.564,P = 0.012）。 结论 CD40基因rs1883832 C/T多态性和TCCA单倍型与SLE的发病有相关性,其中rs1883832 T等位基因可能是SLE的遗传易感基因。     

寻常型鱼鳞病患者皮损中间丝聚合蛋白及其基因的改变

【摘要】 目的 探讨寻常型鱼鳞病患者中间丝聚合蛋白（FLG）基因突变与FLG及兜甲蛋白在寻常型鱼鳞病患者皮损组织中的表达及其临床意义。 方法 采用SP免疫组化方法检测10例汉族寻常型鱼鳞病患者皮损及14例健康对照皮肤组织内FLG及兜甲蛋白的表达,用图像分析软件ImagePro plus（IPP）判定FLG及兜甲蛋白在寻常型鱼鳞病患者皮损及正常皮肤组织中表达的阳性单位（PU值）。提取10例汉族寻常型鱼鳞病患者及100例健康对照者的基因组DNA,采用PCR及直接测序法,对FLG基因已报道的13个突变位点（3321delA、441delA、1249insG、E1795X、S3296X、R501X、2282del4、R2447X、S2889X、7945delA、3702delG、Q2417X、R4307X）进行测序。 结果 FLG在寻常型鱼鳞病皮损及健康对照皮肤角质层、颗粒层、棘层及基底层细胞均有表达,胞质染色多见;寻常型鱼鳞病皮损阳性染色PU值明显低于健康对照皮肤（分别为0.2082 ± 0.0080和0.2300 ± 0.0228,两组比较,t = 3.30,P < 0.01）。兜甲蛋白在寻常型鱼鳞病皮损及健康对照皮肤颗粒层、棘层及基底层细胞均有表达,胞质及胞核染色多见;寻常型鱼鳞病皮损表达的PU值明显低于健康对照皮肤（分别为0.1370 ± 0.0112和0.1493 ± 0.0073,两组比较,t = 3.07,P < 0.01）。7例寻常型鱼鳞病患者检测到FLG 3321delA突变位点,2例检测到FLG 441delA突变位点,健康对照组未检测到FLG基因突变位点。 结论 FLG（3321delA,441delA）可能是汉族寻常型鱼鳞病患者的突变位点之一。FLG及兜甲蛋白表达下降可能与寻常型鱼鳞病患者皮肤屏障功能障碍有关。     

寻常型鱼鳞病一家系Filaggrin基因突变检测

目的探讨一家系寻常型鱼鳞病(ichthyosis vulgaris,IV)丝聚合蛋白(filaggrin,FLG)基因的突变。方法提取IV患者及其家庭成员和100例健康对照者基因组DNA,采用PCR及直接测序法,对FLG基因已报道的13个突变位点(3321delA,441delA,1249insG,E1795X,S3296X,R501X,2282del4,R2447X,S2889X,7945delA,3702delG,Q2417X,R4307X)进行测序。结果三代7位成员中4例IV患者同时检测到FLG(441delA)基因突变。结论患者FLG(441delA)基因突变可能导致其发病。     

温州汉族SLE患者载脂蛋白H基因Leu247Val多态性与抗磷脂抗体的相关性研究

目的 探讨apoH第7号外显子G817T（Leu247Val）的多态性与温州地区汉族SLE患者抗磷脂抗体产生的关系。方法 收集温州地区汉族SLE患者165例及健康体检者160例,PCR技术及DNA测序技术检测apoH第7号外显子G817T（Leu247Val）的多态性;蝰蛇毒试验法测定狼疮抗凝物（LAC）比值,ELISA法测定其抗β2糖蛋白I（β2GPI）抗体及抗心磷脂抗体（ACA）。用Logistic回归分析Leu247Val多态性与抗磷脂抗体（APL）的关系。结果 SLE患者组与健康对照组G817T位点的基因型构成及等位基因频率差异有统计学意义（P值均 < 0.01）,患者组TT、GT基因型及T等位基因频率较高,而GG基因型及G等位基因频率偏低。G817T位点的基因型分布与LAC,抗β2GPI抗体及ACA的阳性均有关（P值 < 0.05,< 0.01,< 0.05）。GT基因型是LAC（P < 0.05,OR = 2.33,95% CI 1.18 ~ 4.59）、抗β2GPI抗体（P < 0.01,OR = 5.92, 95% CI 2.61 ~ 13.46）及ACA（P < 0.05,OR = 2.52,95% CI 1.22 ~ 5.24）产生的危险因素。TT基因型是抗β2GPI抗体的危险因素（P < 0.01,OR = 5.84,95% CI 1.69 ~ 20.20）。结论 温州地区汉族SLE患者apoH第7号外显子G817T（Leu247Val）位点的多态性与APL产生有关,GT、TT基因型是APL产生的危险因素。     

雌激素受体-α基因多态性与白癜风相关性研究

目的探讨雌激素受体-α(ER-α)基因多态性与白癜风的相关性。方法应用PCR-RFLP分析技术,检测690例汉族白癜风患者和700例汉族对照者ER-α基因内含子1PvuⅡT/C和XbaIA/G酶切位点基因多态性。结果白癜风组与对照组之间C/T基因型频率(P=0.000)差别有显著性意义,其C等位基因频率亦明显高于对照组(P=0.000,OR1.33,95%CI1.14~1.51);女性患者C/T基因型频率(P=0.001)、C等位基因频率(P=0.002,OR1.41,95%CI1.13~1.75)亦明显高于女性对照组;男性患者和男性对照组C等位基因频率(P=0.043,OR1.25,95%CI1.01~1.56)差别有显著性意义;ER-α基因内含子1XbaⅠA/G酶切多态性男性患者G等位基因频率(P=0.040,OR1.32,95%CI1.01~1.71)明显高于男性对照组;其余各组间差别无显著性意义(P>0.05)。结论ER-α基因PvuII酶切多态性与白癜风存在相关性,携带C等位基因的女性患者更易患白癜风。XbaI酶切多态性可能与男性白癜风患者之间存在相关性。提示ER-α可能是白癜风患者易感性的备选因素。     

红斑狼疮患者1006例临床特征研究:来自中国人群红斑狼疮多中心病例对照研究(LEMCSC)

目的 探讨中国红斑狼疮(LE)患者的临床特征.方法 从中国人群LE多中心病例对照研究(LEMCSC)中获得数据,以统一标准纳入样本及收集临床资料.用EpiData 3.1录入数据和SPSS 18.0统计数据.结果 共有1 006例LE患者(女性87.6％)纳入分析,其中系统性红斑狼疮(SLE) 887例(女性89.9％),无内脏系统受累的皮肤型红斑狼疮(CLE) 119例(女性70.6％).SLE患者各系统受累情况是皮肤(72.7％)＞关节(69.2％)＞血液(60.8％)＞肾脏(48.5％)＞浆膜(18.2％)＞神经系统(5.7％).LE特异性皮损的出现可增加伴发关节炎风险[OR=1.612,95％可信区间(CI)1.181 ～ 2.200],却可降低伴发肾炎和浆膜炎的风险(OR分别为0.218及0.311;95％ CI分别为0.157 ～ 0.303及0.218 ～ 0.443).急性皮肤型红斑狼疮皮损的出现是伴发系统受累的危险因素(OR=4.931,95％ CI 3.232 ～ 7.524),而慢性皮肤型红斑狼疮皮损的出现却是伴发系统受累的保护因素(OR=0.355,95％ CI 0.234 ～ 0.541).LE非特异性皮损的出现与内脏受累密切相关.结论 揭示中国LE患者的基本临床特征以及LE相关皮损与内脏器官受累的关系.     

白介素27基因多态性与广西壮族系统性红斑狼疮的相关性研究

目的 探讨白介素27（IL-27）基因单核苷酸多态性与广西壮族系统性红斑狼疮（SLE）易感性之间的关系。方法 以135例SLE患者和150例正常人对照者为研究对象,应用聚合酶链反应-限制性片段长度多态性和DNA测序的方法对IL-27基因-964 A/G、2905 T/G单核苷酸多态性进行基因分型。结果 SLE组和正常人对照组中IL-27基因2905 T/G多态性分布差异无统计学意义（χ2 = 1.63,P > 0.05）,而IL-27基因-964 A/G多态性的分布差异有统计学意义（χ2 = 9.88,P < 0.01）。等位基因频率的相对风险分析发现,-964 G等位基因携带者患SLE的风险是-964 A等位基因的1.725倍（OR = 1.725,95% CI：1.227 ～ 2.425）。联合基因型分析发现,IL-27的-964 G /2905 G等位基因频率SLE组（10.7%）显著高于对照组（5.3%）（P < 0.01）,-964 G/2905 G等位基因携带者显著增加了SLE的发病风险（OR = 2.351,95% CI：1.228 ～ 4.501）。结论 IL-27基因-964 A/G多态性与SLE的发病具有相关性,其中-964 G等位基因可能是SLE的遗传易感基因。     

Filaggrin mutations in children with severe atopic dermatitis

Atopic dermatitis (AD) results from strong genetic and environmental interactions. AD shows genetic linkage to Chromosome 1q21. This region contains the epidermal differentiation complex (EDC), which consists of genes that form essential components of epidermal surfaces. Filaggrin (FLG) is one of these. Mutations in FLG/(R501X and 2282del4) are reported to be strongly associated with AD and to influence asthma accompanying AD. We investigated these effects in families recruited through a child with severe AD. We genotyped two panels of families, totalling 426, containing 990 affected and unaffected children. We found significant associations with AD (P=0.0001), asthma (P=0.006), and atopy (P=0.002). The FLG mutations were present in 26.7% of patients with AD, but were also present in 14.4% of children without AD. They were weakly associated with disease severity. The variants were not independently associated with asthma. The overall LOD score for genetic linkage of markers to the region was 3.57. This fell to 2.03 after accounting for the FLG mutations, indicating the presence of other genetic variants influencing AD at this locus. Our results provide further confirmation of the importance of mutations in FLG and the skin barrier in AD pathogenesis. The results indicate that investigations of other genes within the EDC should be undertaken.     

Kontaktallergie und Atopie

Retrospective studies demonstrate that the prevalence of skin sensitization does not significantly differ between atopic and non-atopic patients. In children and adolescents the risk for sensitization seems to occur independently from AD. According to the results of a recent study, AD patients are overrepresented in the group of polysensitized patients. IgE-mediated sensitization as well as an early onset of AD and duration of the disease have been identified as possible risk factors for skin sensitization to contact allergens. A defective permeability barrier with increased epidermal water loss is a hallmark of AD and contributes to sensitization against common allergens. A highly significant association between FLG mutations and the risk of early onset, severe, persistent AD and an increased risk for asthma has been shown in several studies. A more recent study revealed an association between FLG mutations and increased nickel sensitization, but not other contact allergens. However, further large prospective studies with well-characterized patients are necessary to clarify the correlation between impaired skin barrier, atopic dermatitis and allergic contact dermatitis.     

Specific filaggrin mutations cause ichthyosis vulgaris and are significantly associated with atopic dermatitis in Japan

Mutations in the gene encoding filaggrin (FLG) have been identified as the cause of ichthyosis vulgaris (IV) and shown to be major predisposing factors for atopic dermatitis (AD). However, these studies have been mainly carried out in European populations. In early 2007, we identified two Oriental-specific FLG mutations in four Japanese families with IV and reported that filaggrin mutations were also significant predisposing factors for AD in Japan. However, the frequency of FLG mutations observed in our Japanese AD cohort (5.6%), was much lower than that seen in Europeans (up to 48%). Here, we studied a further seven Japanese families with IV and identified two additional nonsense mutations in FLG, S2889X, and S3296X. We found that more than 20% of patients in our Japanese AD case series carry FLG mutations, and there is significant statistical association between the four mutations and AD (chi(2) P=8.4 x 10(-6); heterozygote odds ratio 7.57, 95% CI 2.84-23.03). These data emphasize that skin-barrier impairment due to reduced filaggrin expression plays an important role in the pathogenesis of AD and sheds further light on the genetic architecture of atopy in Japan.     

系统性红斑狼疮患者皮肤血管炎的临床研究

目的 比较有无皮肤血管炎表现的系统性红斑狼疮(SLE)患者的临床和实验室特点,探讨SLE患者皮肤血管炎与实验室指标以及内脏损伤的关系.方法 分析2011年7月至2014年10月复旦大学附属华山医院皮肤科收治的152例有皮肤症状的SLE患者临床和实验室资料,并将其分为四肢末端血管炎组和网状青斑组.应用logistic回归模型分析皮肤血管炎与临床和实验室各变量的关系.结果 152例SLE患者中,62例(41％)有皮肤血管炎表现(包括55例四肢末端血管炎和7例网状青斑),90例(59％)无皮肤血管炎.四肢末端血管炎组患者年龄(30.54±12.67)岁、24 h尿蛋白定量和血清尿素异常升高分别为39.39％和2.08％.均明显低于无血管炎组年龄(37.77±12.17)岁,64.00％和16.43％,而女性比例(98.18％)、头颅MRI异常(37.50％)、贫血(87.03％)、抗核糖体P蛋白抗体阳性的比例(77.77％)及SLEDAI指数(14.71±7.75)均明显高于无血管炎组(84.44％、12.19％、70.93％、53.65％、10.68±5.61),差异有统计学意义(均P＜0.05),而C3降低的比例与无血管炎组相比差异无统计学意义(P=0.362).网状青斑组患者C3降低的比例(28.57％)显著低于无血管炎组(79.76％,P=0.008),其他指标与无血管炎组相比,差异无统计学意义(均P＞0.05).体质指数(BMI)、肺功能异常及其他实验室指标在四肢末端血管炎组、网状青斑组及无血管炎组间差异无统计学意义(均尸＞ 0.05).logistic回归分析显示,在排除了年龄和性别的影响后,皮肤血管炎与头颅MRI异常(OR=4.24,95％CI:1.17 ～ 16.13,P=0.028)及抗核糖体P蛋白抗体阳性(OR=3.97,95％ CI:1.86 ～ 8.47,P=0.0004)呈显著正影响的关系;与24 h尿蛋白异常呈显著负影响的关系(OR=0.25,95％ CI:0.09～ 0.69,P=0.009);与血清尿素异常(OR=0.12,95％ CI:0.01 ～ 1.06)、C3降低(OR=0.93,95％ CI:0.38 ～ 2.28)、贫血(OR=1.38,95％ CI:0.56～3.40)及SLEDAI(OR=1.05,95％ CI:0.98～1.14)则无显著影响关系(均P＞0.05).结论 皮肤血管炎与SLE中枢神经系统损伤及抗核糖体P蛋白抗体的产生密切相关,对具有此类皮肤损伤的SLE患者,应密切监测中枢神经系统损伤情况.无皮肤血管炎的SLE患者发生肾脏损伤的概率较大,也需加强监测.     

Polymorphisms within the CTLA4 gene are associated with infant atopic dermatitis

BACKGROUND: Atopic dermatitis (AD) is one of the most common childhood disorders. It can have a significant impact on the physical and psychological well-being of affected individuals. Although environmental triggers are important, AD also has a strong genetic component. Identifying genes associated with AD may help to understand better the basis of this disorder and its relationship with other allergic disorders such as asthma. OBJECTIVES: Polymorphisms in the gene encoding the inhibitory CTLA4 receptor, an important regulator of T cells, are associated with asthma as well as autoimmune disorders. We have now tested whether polymorphisms in the CTLA4 gene are also associated with early childhood AD. METHODS: A family-based cohort of 112 children and their parents was recruited from Western Sydney, Australia. All children were seen by a paediatric dermatologist and presented with AD within the first 3 years of life. Using the transmission disequilibrium test, individual and haplotypic associations with the +49 and CT60 polymorphisms in exon 1 and the 3' nontranslated DNA of the CTLA4 gene were tested. RESULTS: Single tests of association revealed significant association of the +49(A) [P = 0.037, odds ratio (OR) 1.59, 95% confidence interval (CI) 1-2.55] and borderline significance of the CT60(A) alleles (P = 0.055, OR 1.51, 95% CI 1-2.38). Significant association of the +49(A)/CT60(A) haplotype was detected (P = 0.002, OR 1.78, 95% CI 1.2-2.65). CONCLUSIONS: Polymorphisms within the gene encoding CTLA4 were associated with early onset infant AD. This is in agreement with findings from asthmatic cohorts, suggesting that the +49(A)/CT60(A) haplotype is a genetic risk factor common to asthma and AD.     

长脉冲1064 nm Nd∶YAG激光治疗婴儿血管瘤5年回顾分析

目的 评价长脉冲1064 nm Nd∶YAG激光治疗婴儿血管瘤的临床效果和特点.方法 吉林大学第一医院皮肤科门诊接受1064 nm Nd∶YAG激光治疗的资料完整的婴儿血管瘤病例共794例(900处血管瘤),回顾性分析患者临床资料,包括患者年龄、性别,血管瘤发生时间、病程、类型、位置、面积、并发症及治疗结果.不同性别间的疗效比较采用两组秩和检验;不同疗效患儿的年龄和血管瘤的面积采用中位数±四分位数间距进行描述,组间比较采用多组秩和检验;不同血管瘤的位置和不同血管瘤分类间的疗效比较均采用多组秩和检验;影响血管瘤疗效的多因素分析方法采用有序多分类logistic回归法.结果 794例患儿经1～5次激光治疗后,总有效率为87.56％(788/900).疗效与患儿的性别(Z=-7.18,P＞ 0.05)和血管瘤的位置(x2=2.34,P＞ 0.05)无关,而主要与患儿的年龄(x2=103.131,P＜ 0.001)和血管瘤类型(x2=107.709,P＜ 0.001)相关.年龄越大,疗效越好(OR=1.21,95％ CI 1.14～ 1.28,P＜0.001);同单纯血管瘤比较,混合型血管瘤疗效最差(OR=0.22,95％ CI0.17～ 0.29,P＜0.001),其次为深层血管瘤(OR=0.30,95％ CI0.10～0.93,P=0.037).不良反应包括术后水疱、萎缩性瘢痕、色素沉着、色素减退、皮肤质地改变,未见增生性瘢痕.结论 1064 nm Nd:YAG激光是治疗各种类型早期婴儿血管瘤的有效手段之一.     

Sequence analysis of filaggrin gene by novel shotgun method in Japanese atopic dermatitis

BACKGROUND: Recent reports indicated that nonsense mutations in filaggrin (FLG) found in ichthyosis vulgaris (IV) patients are predisposing factors for atopic dermatitis (AD) with asthma. The exon 3 of FLG contains tandemly repeated, highly homologous, 11-13 sequence units of 972 or 975 bp, each of which corresponds to the coding sequence of the processed filaggrin with slight sequence difference. This unique gene structure has hampered the precise DNA sequence determination. OBJECTIVE: We developed a novel DNA sequencing method "FLG-shotgun" to directly characterize the mutations in Japanese AD patients. METHODS: We examined 24 Japanese AD patients with "FLG-shotgun" method. RESULTS: Multiple units of FLG were amplified by PCR using several sets of common primers for the conserved regions, and DNA sequences of each cloned PCR product were determined. Multiple reads of DNA sequences in both alleles were aligned and re-constructed to cover the entire coding regions. We found three major genotypes (A, B, and C) which represent different numbers (11-13) of homologous sequence units. Furthermore, we found two novel nonsense mutations; one mutation 8666-8667CC>GA on the unit 9 of allele B that causes a nonsense mutation S2899X in two patients and the other mutation 9887C>A on the unit 10 of allele B that causes a nonsense mutation S3296X in two patients. CONCLUSION: We found two novel FLG mutations by directly analyzing Japanese patients with AD. FLG-shotgun will provide a valuable tool to further define the nature of the AD phenotype associated with FLG mutations.     

Lidocaine inhibits staphylococcal enterotoxin-stimulated activation of peripheral blood mononuclear cells from patients with atopic dermatitis

Atopic dermatitis (AD) is an inflammatory, chronically relapsing, pruritic skin disease and lesions associated with AD are frequently colonized with Staphylococcus aureus (S. aureus). Activation of T cells by staphylococcal enterotoxins (SE) plays a crucial role in the pathogenesis of AD. Previous studies have demonstrated that lidocaine could attenuate allergen-induced T cell proliferation and cytokine production in peripheral blood mononuclear cells (PBMCs) from asthma patients. The purpose of this study was to investigate the effects of lidocaine on SE-stimulated activation of PBMCs from AD patients. PBMCs were isolated from ten AD patients and stimulated by staphylococcal enterotoxin A (SEA) or staphylococcal enterotoxin B (SEB) in the presence or absence of lidocaine in various concentrations. Cellular proliferation and the release of representative T_H1- and T_H2-type cytokines were measured. The effect of lidocaine on filaggrin (FLG) expression in HaCaT cells co-cultured with SE-activated PBMCs was also examined. Our results demonstrated that lidocaine dose-dependently inhibited the proliferative response and the release of IL-4, IL-5, IL-13, TNF-α, and IFN-γ from SEA- and SEB-stimulated PBMCs and also blocked the down-regulation of FLG expression in HaCaT cells co-cultured with SEA- and SEB-activated PBMCs. These results indicate that lidocaine inhibited SEA- and SEB-stimulated activation of PBMCs from patients with AD. Our findings encourage the use of lidocaine in the treatment of AD.