牛奶诱导的嗜酸性食管炎患者激活的TH2细胞和牛奶特异性TH2细胞表达增加
2018/01/08
摘要
背景:嗜酸性食管炎(EoE)是一种过敏性炎症性的疾病,是由食品过敏原并以进行性食管功能障碍为特征。食管活检标本有嗜酸性粒细胞和TH2细胞因子的表达。
目的:确定TH2细胞是否可以在牛奶诱导的嗜酸性食管炎患者外周血中存在。
方法:在喝牛奶的激活EoE(EoE-A)期间和不喝牛奶的非激活EoE(EoE-I)期间收集20个患有牛奶诱导的嗜酸性食管炎的孩子和8个作为对照的健康的没有EoE的患者的外周血单核细胞。分析这些样本的T细胞表型,包括细胞内细胞因子孵化牛奶抗原前和孵化牛奶抗原后，并通过流式细胞术进行评估。
结果:与对照组相比，我们发现EoE-A患者的外周血中CD4+ TH2细胞显著增加。此外, 与对照组(0.034%[0.007%]) 和 EoE-I患者 (0.025% [0.008%])相比，我们发现激活标记CD154+ T细胞的平均数（标准方差）在EoE-A患者(0.17% [0.047%])中显著增长。与对照组和 EoE-I患者相比，这些CD4+T细胞表达的TH2细胞因子(白细胞介素4、5、13)显著增加。牛奶抗原使CD3+CD4+CD154+IL-5+细胞显著增加：牛奶诱导的EoE-A(0.050% [0.008%] to 0.079% [0.017%]) ，EoE-I (0.0045% [0.002%] to 0.014% [0.008%]) ，对照组(0.008% [0.003%] to 0.003% [0.001%])。
结论:我们的研究结果表明,EoE患者外周血中的T细胞可以被牛奶过敏原特异性激活。
Elevated expression of activated TH2 cells and milk-specific TH2 cells in milk-induced eosinophilic esophagitis.
CianferoniA(1), Ruffner MA(2), Guzek R(3), Guan S(3), Brown-Whitehorn T(1), Muir
A(4), Spergel JM(5).
Abstract
BACKGROUND:Eosinophilic esophagitis (EoE) is an allergic inflammatory diseasethat is triggered by food allergens and characterized by progressive esophagealdysfunction. Esophageal biopsy specimens are characterized by eosinophilia andexpression of TH2 cytokines.
OBJECTIVE:To ascertain whether TH2 cells can exist in the peripheral blood inpatients with milk-induced EoE.
METHODS: Peripheral blood mononuclear cells from 20 children with milk-inducedEoE were collected during active EoE (EoE-A) while consuming milk and inactiveEoE (EoE-I) while not consuming milk, and 8 healthy patients without EoE wereused as controls. The samples were analyzed for T-cell phenotype, includingintracellular cytokines before and after incubation with milk antigens andassessed by flow cytometry.
RESULTS: We found a significant increase in CD4+ TH2 cells in the peripheralblood of patients with EoE-A compared with the controls. Furthermore, we observeda significant mean (SD) increase in the activation marker of CD154+ T cells(0.17% [0.047%]) in patients with EoE-A compared with control patients (0.034%[0.007%]) and EoE-I (0.025% [0.008%]). These CD4+ T cells expressed significantly increase levels of TH2 cytokines (interleukins 4, 5, and 13) compared with theEoE-I and control groups. CD3+CD4+CD154+IL-5+ cells were significantly increased by milk antigens in both milk-induced EoE-A (0.050% [0.008%] to 0.079% [0.017%]) and EoE-I (0.0045% [0.002%] to 0.014% [0.008%]) compared with the controls(0.008% [0.003%] to 0.003% [0.001%]).
CONCLUSION:Our findings indicate that in EoE peripheral T cells have specificactivation to milk allergens.
背景:嗜酸性食管炎(EoE)是一种过敏性炎症性的疾病,是由食品过敏原并以进行性食管功能障碍为特征。食管活检标本有嗜酸性粒细胞和TH2细胞因子的表达。
目的:确定TH2细胞是否可以在牛奶诱导的嗜酸性食管炎患者外周血中存在。
方法:在喝牛奶的激活EoE(EoE-A)期间和不喝牛奶的非激活EoE(EoE-I)期间收集20个患有牛奶诱导的嗜酸性食管炎的孩子和8个作为对照的健康的没有EoE的患者的外周血单核细胞。分析这些样本的T细胞表型,包括细胞内细胞因子孵化牛奶抗原前和孵化牛奶抗原后，并通过流式细胞术进行评估。
结果:与对照组相比，我们发现EoE-A患者的外周血中CD4+ TH2细胞显著增加。此外, 与对照组(0.034%[0.007%]) 和 EoE-I患者 (0.025% [0.008%])相比，我们发现激活标记CD154+ T细胞的平均数（标准方差）在EoE-A患者(0.17% [0.047%])中显著增长。与对照组和 EoE-I患者相比，这些CD4+T细胞表达的TH2细胞因子(白细胞介素4、5、13)显著增加。牛奶抗原使CD3+CD4+CD154+IL-5+细胞显著增加：牛奶诱导的EoE-A(0.050% [0.008%] to 0.079% [0.017%]) ，EoE-I (0.0045% [0.002%] to 0.014% [0.008%]) ，对照组(0.008% [0.003%] to 0.003% [0.001%])。
结论:我们的研究结果表明,EoE患者外周血中的T细胞可以被牛奶过敏原特异性激活。
(中日友好医院呼吸与危重症医学科 禹汶伯 摘译 林江涛 审校)
(Ann Allergy Asthma Immunol. 2017 Dec 28. pii: S1081-1206(17)31266-8. doi: 10.1016/j.anai.2017.11.006. [Epub ahead of print] )
(Ann Allergy Asthma Immunol. 2017 Dec 28. pii: S1081-1206(17)31266-8. doi: 10.1016/j.anai.2017.11.006. [Epub ahead of print] )
Elevated expression of activated TH2 cells and milk-specific TH2 cells in milk-induced eosinophilic esophagitis.
CianferoniA(1), Ruffner MA(2), Guzek R(3), Guan S(3), Brown-Whitehorn T(1), Muir
A(4), Spergel JM(5).
Abstract
BACKGROUND:Eosinophilic esophagitis (EoE) is an allergic inflammatory diseasethat is triggered by food allergens and characterized by progressive esophagealdysfunction. Esophageal biopsy specimens are characterized by eosinophilia andexpression of TH2 cytokines.
OBJECTIVE:To ascertain whether TH2 cells can exist in the peripheral blood inpatients with milk-induced EoE.
METHODS: Peripheral blood mononuclear cells from 20 children with milk-inducedEoE were collected during active EoE (EoE-A) while consuming milk and inactiveEoE (EoE-I) while not consuming milk, and 8 healthy patients without EoE wereused as controls. The samples were analyzed for T-cell phenotype, includingintracellular cytokines before and after incubation with milk antigens andassessed by flow cytometry.
RESULTS: We found a significant increase in CD4+ TH2 cells in the peripheralblood of patients with EoE-A compared with the controls. Furthermore, we observeda significant mean (SD) increase in the activation marker of CD154+ T cells(0.17% [0.047%]) in patients with EoE-A compared with control patients (0.034%[0.007%]) and EoE-I (0.025% [0.008%]). These CD4+ T cells expressed significantly increase levels of TH2 cytokines (interleukins 4, 5, and 13) compared with theEoE-I and control groups. CD3+CD4+CD154+IL-5+ cells were significantly increased by milk antigens in both milk-induced EoE-A (0.050% [0.008%] to 0.079% [0.017%]) and EoE-I (0.0045% [0.002%] to 0.014% [0.008%]) compared with the controls(0.008% [0.003%] to 0.003% [0.001%]).
CONCLUSION:Our findings indicate that in EoE peripheral T cells have specificactivation to milk allergens.
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