急性脑梗死患者血清白介素-18和组织因子水平变化及其与凝血功能的关系

目的 探讨急性脑梗死(ACI)患者血清白介素(IL)-18和组织因子(TF)水平的变化及其与凝血功能关系.方法 79例ACI患者(ACI组)于入院次日、25名健康体检者(正常对照组)于体检当日早晨,分别检测血清IL-18、TF水平和凝血功能.结果 ACI组患者的血清IL-18、TF水平[(282.22±127.45)pg/ml,(2.10±1.23)ns/ml]明显高于正常对照组[(131.13±37.17)pg/ml,0.67±0.34)ng/ml](P<0.01～0.001):ACI组患者凝血功能指标中的部分凝血活酶时间及纤维蛋白原(Fib)水平显著高于正常对照组(均P<0.05);ACI组患者血清TF水平与凝血酶原时间及Fib水平呈正相关(r=0.376,r=0.473,P<0.05～0.01).结论 血清IL-18与TF水平异常增高是参与动脉粥样硬化相关性血栓形成的重要原因之一,抗凝及降纤治疗通过抑制TF水平逆转该病理过程.     

颈动脉内中膜厚度与血清白介素-6、白介素-18水平的关系

目的 探讨颈动脉内中膜厚度(IMT)与血清细胞因子白介素 (IL)-6、IL-18水平的关系. 方法选择40例短暂性脑缺血发作(TIA)患者(TIA组)、64例急性脑梗死(ACI)患者(ACI组)和30名健康对照者(正常对照组),分别测量其颈动脉IMT值,并分为IMT＜1.0 mm亚组和IMT≥1.0 mm亚组.利用液相平衡竞争放射免疫分析法(RIA)和酶联免疫吸附法(ELISA)分别测定3组的血清IL-6和IL-18水平,并对IMT与IL-6、IL-18的关系进行分析. 结果 TIA组和ACI组所有IMT≥1.0 mm患者血清IL-6、IL-18含量[TIA组分别为(141.61±27.86)pg/ml和(212.42±51.88)pg/ml;ACI组分别为(157.94±27.98)pg/ml和(224.99±59.56)pg/ml]比正常对照组[(101.41±35.56)pg/ml和165.87±29.89)pg/ml]升高(P<0.05～0.01); TIA组、ACI组IMT≥1.0 mm亚组患者血清IL-6、IL-18含量和IMT<1.0 mm亚组[TIA组分别为(141.61±27.86, 212.42±51.88)pg/ml和(108.48±35.56,170.98±29.83)pg/ml;ACI组分别为(157.94±27.98,224.99±59.56) pg/ml和(129.56±35.56,195.07±29.86)pg/ml]二者有显著差异(均P<0.05).TIA组、ACI组IMT≥1.0 mm亚组患者IMT与血清IL-18含量呈正相关(r＝0.549,P<0.01),与血清IL-6含量无相关性((r＝0.304,P＝0.057). 结论 TIA组、ACI组IMT增厚的患者血清IL-6、IL-18的水平升高;IMT的增厚与血清IL-18含量呈正相关.推测IL-6、 IL-18可能参与了动脉硬化的形成过程.     

白介素-4 C590T基因多态性与血清白介素-4水平及动脉粥样硬化性血栓性脑梗死的关系

目的探讨白介素(IL)-4C590T基因多态性与血清IL-4水平以及动脉粥样硬化性血栓性脑梗死(ATCI)的关系。方法采用PCR-限制性片段长度多态性(PCR-RFLP)方法检测159例ATCI患者和151名健康正常对照者的IL-4C590T基因的单核苷酸多态性,用酶联免疫吸附(ELISA)法检测正常对照组的血清IL-4水平。结果正常对照组IL-4C590T基因TT型的血清IL-4水平[(31.85±5.68)pg/ml]显著高于TC型[(28.67±6.00)pg/ml]和CC型[(20.98±0.99)pg/ml],TC型又显著高于CC型(均P<0.01)。ATCI组与正常对照组IL-4C590T基因型和等位基因频率的分布差异无统计学意义(均P>0.05)。结论IL-4590T等位基因与高血清IL-4水平有关,IL-4C590T基因多态性与ATCI的发病无明显关系。     

丙种球蛋白对格林-巴利综合征患者白介素12与白介素18表达的影响及其相关性研究

目的探讨丙种球蛋白治疗对格林-巴利综合征(GBS)对患者体内白介素12(IL12)和白介素18(IL18)的表达的影响。方法用ELISA方法对静脉注射丙种球蛋白(IVIG)治疗GBS前后的血清、脑脊液IL12和IL18表达,同时用RT-RCR法检测血淋巴细胞白介素12受体(IL12R)mRNA与IL18RmRNA的表达。结果17例GBS治疗前血清IL12含量为45.6±12.2pg/ml,治疗后为17.1±4.74pg/ml(P<0.01);IL18治疗前为157.5±39.3pg/ml,治疗后为126.2±22.6pg/ml。5例GBS治疗前脑脊液IL12为25.2±5.8pg/ml,治疗后为16.7±3.6pg/ml。IL-18治疗前为121.8±27.9pg/ml,治疗后为53.6±15.6pg/ml。17例GBS治疗前血淋巴细胞表面受体IL-12RmRNA的表达强度为0.2948±0.098,治疗后为0.1507±0.087,与治疗前比显著降低(P<0.05)。治疗前血淋巴细胞IL18RmRNA表达强度为0.5352±0.1134,治疗后为0.2843±0.1127,与治疗前比显著降低(P<0.05)。IL12与IL18蛋白在血清中的表达呈显著正相关;IL12与IL18淋巴细胞表面受体mRNA的表达呈显著正相关。结论丙种球蛋白治疗能够下调GBS患者IL12与IL18的表达。     

Guillain-Barré综合征患者血清和脑脊液IL-18、IL-13水平的测定及临床意义

目的探讨IL-18、IL-13在吉兰-巴雷(GBS)患者血清和脑脊液(CSF)中的含量变化及其在发病机制中的作用。方法用酶联免疫吸附法(ELISA)测定GBS患者急性期与恢复期血清及脑脊液IL-18、IL-13水平。结果GBS患者急性期血清及脑脊液IL-18与IL-13水平均明显高于恢复期和对照组(均P<0·01);且病情重者高于病情轻者(均P<0·05);恢复期血清IL-18、IL-13水平虽下降,但仍高于对照组(均P<0·01);相关分析发现血清和脑脊液IL-18、IL-13呈正相关关系(均P<0·05)。结论IL-18、IL-13可能在周围神经脱髓鞘的病理损害的发病机制中起着十分重要的作用,并与病情轻重有关。     

新生儿缺氧缺血性脑病血清IL-18和TNF-α的水平及意义

目的探讨新生儿缺氧缺血性脑病(HIE)血清中白介素-18(IL-18)和肿瘤坏死因子-α(TNF-α)的水平及临床意义。方法采用双抗体夹心ELISA法检测37例HIE患儿和15例正常新生儿血清中IL-18、TNF-α的水平。结果 HIE患儿血清中IL-18、TNF-α水平急性期和恢复期均高于正常新生儿同期水平(P<0.05)。轻、中、重度HIE患儿急性期和恢复期血清中IL-18、TNF-α水平比较差异均有统计学意义(P<0.05)。不同程度HIE患儿的急性期和恢复期血清中IL-18、TNF-α水平比较差异有统计学意义(P<0.05)。结论 IL-18、TNF-α可能参与了HIE的病理生理学过程,两者水平检测可用于HIE的病情评估。     

重症肌无力患者血清可溶性Fas水平变化及其临床意义

目的探讨重症肌无力(MG)患者血清可溶性Fas(sFas)水平变化及其临床意义。方法采用流式细胞术及酶联免疫吸附法(ELISA)分别测定45例MG患者(MG组)及40例对照者(对照组)外周血T细胞亚群分布和血清sFas水平,并对其中24例MG患者应用糖皮质激素(GC)治疗前后的血清sFas水平进行比较。结果(1)MG组外周血中CD8 T细胞百分率为(21.50±2.21)%,明显低于对照组[(27.75±3.00)%](P<0.01);CD4 /CD8 比值(1.92±0.26)明显高于对照组(1.48±0.16)(P<0.01);血清sFas水平[(3542.06±706.23)pg/m l]显著高于对照组[(2568.18±562.48)pg/m l](P<0.01)。(2)MG组全身型血清sFas水平为(3914.23±804.81)pg/m l,极明显高于眼肌型[(2797.72±592.83)pg/m l](P<0.001);病情中、重度患者明显高于病情轻度者(均P<0.005);预后良好者[(3254.69±661.73)pg/m l]显著低于预后不良者[(4178.38±841.65)pg/m l](P<0.001)。(3)24例MG患者经GC治疗后sFas水平[(2864.59±617.43)pg/m l]较治疗前[(3539.67±705.92)pg/m l]极显著降低(P<0.001)。结论MG患者血清凋亡抑制因素sFas水平增高,并与MG类型、病情及预后相关;GC治疗可以改善MG患者的免疫功能。     

急性期Guillain-Barr(e)综合征患者人类肿瘤坏死因子样分子1A表达与T细胞分泌γ-干扰素水平的关系

目的 探讨人类肿瘤坏死因子样分子1A(hTL1A)在急性期Guillain-Barre综合征(GBS)中表达及其与T细胞分泌γ-干扰素(IFN-γ)水平的关系.方法 ①重组人可溶性hTL1A(rhsTL1A)免疫6周龄雌性Bal b/c小鼠,用人脐带静脉内皮细胞(HUVECs)以免疫荧光染色法鉴定rhsTL1A抗血清.②鉴定rhsTL1A的生物学活性:健康捐赠者外周血单个核细胞(PBMCs)接种于96孔板,设2 μg/ml植物血凝素(PHA)、2 μg/ml PHA+25 ng/ml rhsTL1A、2 μg/ml PHA+100 ng/mlrhsTL1A、2 μg/ml PHA+400 ng/ml rhsTL1A组,~3H-TdR掺入法检测T细胞增殖.③酶联免疫吸附(ELISA)法检测急性期GBS患儿血清中IFN-γ水平.④流式细胞术检测急性期GBS患儿外周血中CD_3~+ hTL1A~+ T/CD_3~+ T细胞的百分比.⑤分离急性期GBS患儿PBMCs,给予2 μg/ml PHA和400ng/ml rhsTL1 A,培养72 h后ELISA法检测IFN-γ水平.结果 ① rhsTL1A抗血清能够识别真核细胞HUVECs表达hTL1A.②T细胞增殖实验结果显示各组刺激指数(SI)均较对照组升高,400 ng/mlrhsTL1A组的SI最大(2.65).③急性期GBS患儿血清IFN9-γ水平[(102.25±22.17)pg/ml]较对照组[(28.75±1.31)pg/ml]显著升高(t=3.309,P<0.05).④急性期GBS患儿外周血中CD_3~+TL1A~+T/CD_3~+ T细胞比例(18.22%±1.83%)较健康对照组(5.17%±0.48%)显著增高(t=6.884,P<0.01).⑤健康对照组和急性期GBS组PBMCs经2 μmg/ml PHA和400 ng/ml rhsTL1A孵育后,IFN-γ分泌量[(43.56±4.41)pg/ml、(180.64±38.39)pg/ml]均显著增高(t=4.523、2.600,P<0.01、0.05),并且急性期GBS组的IFN-γ水平显著高于健康对照组(t=3.545,P<0.05).结论 ①400 ng/ml rhsTL1A能有效促进2μg/ml PHA活化的T细胞增殖,rhsTL1A具有生物学活性.②急性期GBS患儿外周血中活化T细胞表达hTL1A增加,可通过与其受体DR_3相互结合,促进IFN-γ的分泌.     

脑梗死患者血清细胞因子和C-反应蛋白水平的变化及其意义

目的观察脑梗死(CI)患者血清细胞因子——白介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α)及C-反应蛋白(CRP)水平的变化及其意义。方法应用放射免疫法测定合并糖尿病(DM)CI患者(DMCI组,30例)、非DM的CI患者(NDMCI组,30例)、DM患者(DM组,20例)和正常对照组(20人)血清IL-1β、IL-6、TNF-α水平;应用免疫比浊法测定血清CRP水平,根据改良爱丁堡+斯堪的那维亚卒中量表神经功能缺损程度评分对CI患者按病情进行分组。结果DMCI组、NDMCI组及DM组血清IL-1β[(0.60±0.04)ng/ml、(0.33±0.03)ng/ml、(0.30±0.02)ng/ml]、IL-6[(231.07±7.68)pg/ml、(141.34±6.50)pg/ml、(118.92±5.82)pg/ml]、TNF-α[(2.70±0.11)ng/ml、(1.85±0.11)ng/ml、(1.21±0.13)ng/ml]及CRP[(7.44±0.26)ml/L、(4.67±0.21)mg/L、(4.54±0.24)mg/L]水平显著高于正常对照组[(0.20±0.03)n...     

稳定期精神分裂症患者血浆白介素-1β 水平及其与症状关系

目的:探讨稳定期精神分裂症患者血浆白介素-1β(IL-1β)水平及其与临床症状的关系。方法:纳入稳定期精神分裂症患者75例(患者组)和健康对照者40名(对照组),采用流式多重蛋白分析技术检测血浆炎症因子IL-1β的浓度,采用阳性与阴性症状量表(PANSS)评定患者临床症状。结果:患者组IL-1β水平[(2.10±0.59)pg/ml]较对照组[(1.90±0.28)pg/ml]高(P0.05);不同性别、是否吸烟、是否有精神疾病家族史患者之间血浆IL-1β水平差异无统计学意义(P均0.05);患者组血浆IL-1β水平与性别、年龄、受教育年限、首次发病年龄、首次住院年龄、总病程、用药剂量(折合氯丙嗪等效剂量)无相关(P均0.05)。患者组血浆IL-1β水平与PANSS中反应缺乏因子(r=-0.24,P=0.05)、偏执性因子(r=-0.36,P=0.00)、激活因子(r=-0.29,P=0.02)呈负相关。结论:稳定期精神分裂症患者血浆IL-1β浓度高于健康对照者,其与临床症状严重程度存在一定联系。     

IL-12/IL-12R system in multiple sclerosis

IL-12/IL-12 receptor (IL-12R) system orchestrates the Th1 pathway of the immune system by maintaining one of the major bridges between innate and adaptive immune responses. Here, we studied both sides of this system in patients with multiple sclerosis (MS) and in controls. MS patients displayed elevated IL-12Rbeta1 and IL-12Rbeta2 expression on PHA-activated T cells compared to healthy subjects. Higher percentages of IL-12Rbeta1 and IL-12Rbeta2 positive T cells in cerebrospinal fluid (CSF) compared to blood were observed both in MS and other neurological diseases (OND). In contrast, numbers of IL-12 secreting blood mononuclear cells (MNC) were similar in MS and controls. The functional importance of high IL-12Rbeta2 in MS was underlined by the finding that IL-12 stimulated IFN-gamma production and proliferation of PHA-activated T cells correlated with levels of IL-12Rbeta2 expression. Our data indicates a dysregulation of the IL-12/IL-12R system in MS. It is suggested that even in the absence of increased IL-12 levels, the net effect of IL-12 might be augmented in MS by elevated expression of its receptor.     

IL-3、IL-6和IL-8在人脑膜瘤中的表达和作用

目的：探讨白细胞介素（IL）－3、IL－6和IL－8在脑膜瘤细胞中的表达和作用，以及体外针对这种生长调节环路抑制脑膜瘤细胞增殖的可行性。方法：原代培养起21例脑膜瘤细胞。采用ABC免疫细胞化学法明确IL－3、IL－6和IL－8在脑膜瘤细胞中的表达，并选用四唑盐（MTT）比色法观察上述细胞因子及IL－3单抗对脑膜瘤细胞增殖的调控作用。结果：脑膜瘤细胞可分泌IL－3、IL－6和IL－8。IL－3和IL－8皆以剂量依赖关系刺激培养脑膜瘤细胞增殖，而IL－8仅在10ng/ml时对脑膜瘤细胞增殖的刺激效应有统计学差异。IL－3单抗以剂量依赖关系分别抑制正常脑膜瘤细胞及50％V／V脑膜瘤培养是取液刺激的脑膜瘤细胞增殖。结论：IL－3、IL－6和IL－8为脑膜瘤自泌细胞因子；IL－3和IL－6刺激体外培养脑膜瘤细胞增殖；IL－3单抗抑制体外培养脑膜瘤细胞增殖，为脑膜瘤的生物治疗提供新 的理论基础。     

白细胞介素2、6、10在猴实验性变态反应性脑脊髓炎发病中的作用

目的 了解血和脑脊液白细胞介素(IL)-2、IL-6、IL-10在猴实验性变态反应性脑脊髓炎(EAE)发病机制和病情转归中的作用,并进一步阐明多发性硬化(MS)发病的免疫学机制.方法 用猴脑制成脑白质匀浆乳化剂,先制作猴EAE模型10只;随机选另1只猴,用完全福氏佐剂(CFA)0.4 ml皮下注射作对照组.然后对 EAE进行临床病情分级和病程分期,并在不同时期收集血和脑脊液的上清液,用酶增敏免疫分析法测定IL-2、IL-6、IL-10的浓度,用配对t检验进行统计学处理.结果 猴EAE发病前后血中IL-2、IL-6、IL-10有轻度变化,IL-2、IL-6发病后较发病前升高,但差异无显著意义.而猴EAE急性期第1、3周脑脊液IL-2(分别为5.0±0.8和5.3±1.2)较发病前(0.7±0.3)明显升高,P值分别为0.045,0.041,恢复期或慢性期IL-6、IL-10明显升高,P值各为0.004 3,0.006 5,差异有显著意义.结论 IL-2正向调节免疫,使EAE猴的病情加重;IL-6、IL-10负向调节免疫,使EAE猴的病情减轻.此结果 对今后研究EAE或MS的免疫学机制可能有重要指导作用.     

IL-2 and IL-4 polymorphisms as candidate genes in schizophrenia

An immune process, characterized by a relative predominance of the T helper–2 (Th2) system and possibly induced by a viral infection,may be involved in the pathophysiology of schizophrenia. In this context, functional polymorphisms in the Interleukin–2 (IL–2) and Interleukin–4 (IL–4) genes appear to be principal candidates for genetic schizophrenia research. Further evidence for these candidate genes comes from several linkage analyses, pointing to susceptibility gene loci on chromosomes 4q and 5q, where the genes coding for IL– 2 and IL–4 are located. We carried out a case–control study including 230 schizophrenic patients and 251 healthy persons, investigating the IL–2 –330 T/G single nucleotide polymorphism (SNP) and the IL–4 –590 C/T SNP. A significant association of the IL–2 –330 TT genotype and of the IL–4 –590 CC genotype with schizophrenia could be identified. Our findings may partly account for the relative predominance of the Th2 system in schizophrenia, although they cannot directly explain this immunological imbalance, but may be related to an altered antiviral immune response in patients with schizophrenia.     

IL-17及IL-17R在人脑胶质瘤中的表达

目的探讨IL-17及IL-17R在人正常脑组织、低级别胶质瘤、高级别胶质瘤中的表达,及其与胶质瘤级别的关系。方法正常脑组织、低级别胶质瘤、高级别胶质瘤标本分别20、23、22例,采用PCR法检测IL-17mRNA,PCR法及原位杂交法检测IL-17RmRNA,免疫组化法检测IL-17蛋白在各组中的表达。结果 IL-17mRNA在各组中仅见微量表达;IL-17RmRNA在各组中的表达无明显差异(P0.05);蛋白IL-17的表达在正常脑组织、低级别胶质瘤、高级别胶质瘤中依次增高,各组间差异均具有统计学意义(P0.05)。结论蛋白IL-17可能在胶质瘤的发生、发展中起重要作用。     

IL-1beta induced changes in hypothalamic IL-1R1 and IL-1R2 mRNA expression in the rat

Interleukin-1 receptor (IL-1R1 and IL-1R2) mRNA expression was detected within the rat hypothalamus, a primary site of IL-1 action, using RT-PCR. Levels of expression were unchanged by cardiac saline-perfusion. However, intracerebroventricular (i.c.v.) administration of IL-1beta caused changes in receptor mRNA expression in non-perfused animals that were profoundly different to those observed in their saline-perfused counterparts. This study demonstrates the importance of perfusing tissue to remove blood cells when determining changes in IL-1 receptor mRNA expression.     

慢性精神分裂症患者血清IL-2、IL-4和IL-10水平及与精神症状的相关性

目的探讨慢性精神分裂症患者血清白细胞介素2(IL-2)、白细胞介素4(IL-4)和白细胞介素10(IL-10)的水平变化及其与精神症状的相关性。方法于2012年12月-2013年10月在广州医科大学附属脑科医院采用抽签法选取符合《国际疾病分类(第10版)》(ICD-10)诊断标准的40例慢性精神分裂症住院患者为患者组,同期通过广告招募64例健康对照者为对照组。采用酶联免疫吸附试验(ELISA)检测两组血清IL-2、IL-4和IL-10水平,采用阳性和阴性症状量表(PANSS)评估患者组的精神症状。结果患者组血清IL-2水平高于对照组[(25.85±6.06)pg/m L vs.(12.63±1.90)pg/m L],差异有统计学意义(P0.05);两组血清IL-4水平[(7.36±1.54)pg/m L vs.(8.76±3.13)pg/m L]和IL-10水平[(4.29±0.87)pg/m L vs.(3.76±1.17)pg/m L]比较,差异均无统计学意义(P均0.05);患者组血清IL-2、IL-4和IL-10水平与病程、住院时长、抗精神病药治疗剂量及PANSS评分均无线性相关(P均0.05)。结论慢性精神分裂症患者的血清IL-2水平高于健康对照者,IL-4和IL-10水平与对照者比较未见差异;IL-2、IL-4和IL-10水平与患者的精神症状未见线性相关性。     

Differential actions of IL-1 alpha and IL-1 beta in glial cells share common IL-1 signalling pathways

The cytokine interleukin (IL)-1 plays important roles in peripheral and central inflammation via the actions of two ligands IL-1 alpha and IL-1beta that bind to the IL-1 type I receptor (IL-1RI) and trigger identical responses. However, some recent evidence suggests that IL-1alpha and IL-1beta may have differential actions in the CNS. The aim of this study was to characterise the molecular mechanisms responsible for their differential actions in the brain. We show that, while IL-1alpha and IL-1beta induce identical IL-1 signalling pathways, IL-1beta is significantly more potent than IL-1alpha in stimulating IL-6 release in primary mixed glia. These data suggest that the differential effects of IL-1alpha and IL-1beta on glial cells are mediated by alternative pathways to the classical IL-1 signalling cascade.     

帕金森病患者IL-2、IL-6、IL-10的检测及临床意义

目的：检测帕金森病（PD）患者血清及脑脊液（CSF）中IL-2、IL-6和IL-10含量,为深入研究细胞免疫与PD的关系及从炎症角度干预提供实验依据.方法：采用双抗体夹心ELISA法测定PD组血清及CSF中IL-2、IL-6和IL-10的含量,并与对照组（同期体检健康者）比较.结果：PD组血清IL-2、IL-6和IL-10含量均高于对照组（ P〈0.01,P〈0.05）;PD组CSF中IL-6含量高于对照组（ P〈0.05）.新发PD患者、服左旋多巴制剂及服非左旋多巴制剂组PD患者血清及CSF中 IL-2、IL-6、IL-10含量与对照组比较,差异均无统计学意义（ P〉0.05）.PD组血清及CSF中IL-2、IL-6、IL-10含量与年龄、病程、Webster评分、Hoehn-Yahr分级分期、UPDRS-Ⅱ和UPDRS-Ⅲ评分间均无相关性.结论：①PD患者存在血清及CSF中IL-2、IL-6和IL-10水平的改变,PD发病与细胞免疫功能失调有关; ②PD细胞免疫状态的改变不能归因于外源性多巴胺的摄入.     

The endocannabinoid anandamide downregulates IL-23 and IL-12 subunits in a viral model of multiple sclerosis: evidence for a cross-talk between IL-12p70/IL-23 axis and IL-10 in microglial cells

Theiler’s virus (TMEV) infection of the central nervous system (CNS) induces an immune-mediated demyelinating disease in susceptible mouse strains and serves as a relevant infection model for human multiple sclerosis (MS). The endocannabinoid system represents a novel therapeutic target for autoimmune and chronic inflammatory diseases due to its anti-inflammatory properties by regulating cytokine network. IL-12p70 and IL-23 are functionally related heterodimeric cytokines that play a crucial role in the pathogenesis of MS. In the present study we showed that the endocannabinoid anandamide (AEA) downregulated the gene expression of IL-12p70 and IL-23 forming subunits mRNAs in the spinal cord of TMEV-infected mice and ameliorated motor disturbances. This was accompanied by significant decreases on the serological levels of IL-12p70/IL-23 and more interestingly, of IL-17A. In contrast, serum levels of IL-10 resulted elevated. In addition, we studied the signalling pathways involved in the regulation of IL-12p70/IL-23 and IL-10 expression in TMEV-infected microglia and addressed the possible interactions of AEA with these pathways. AEA acted through the ERK1/2 and JNK pathways to downregulate IL-12p70 and IL-23 while upregulating IL-10. These effects were partially mediated by CB2 receptor activation. We also described an autocrine circuit of cross-talk between IL-12p70/IL-23 and IL-10, since endogenously produced IL-10 negatively regulates IL-12p70 and IL-23 cytokines in TMEV-infected microglia. This suggests that by altering the cytokine network, AEA could indirectly modify the type of immune responses within the CNS. Accordingly, pharmacological modulation of endocannabinoids might be a useful tool for treating neuroinflammatory diseases.