Gastroenterology: 通过体外消除维甲酸受体-α来校正克罗恩病患者的缺陷T调节细胞功能

2019-05-17 不详 MedSci原创

克罗恩病(CD)的特征在于肠粘膜中效应细胞和调节性T细胞数量和功能的失衡。抗粘连疗法可以使我们研究T调节(Treg)细胞的受损是否与CD的发病机制有关。本项研究还探究了在存在激活其调节活性的因子的情况下,通过离体扩增是否可以将Treg细胞恢复正常功能。

背景与目的
克罗恩病(CD)的特征在于肠粘膜中效应细胞和调节性T细胞数量和功能的失衡。抗粘连疗法可以使我们研究T调节(Treg)细胞的受损是否与CD的发病机制有关。本项研究还探究了在存在激活其调节活性的因子的情况下,通过离体扩增是否可以将Treg细胞恢复正常功能。

方法
研究人员测量了从CD和健康个体(对照)的患者的外周血或固有层分离的Treg细胞上的整联蛋白α4β7的水平。将Treg细胞离体扩增并与雷帕霉素一起孵育,并以维甲酸受体-α(RARA)的激动剂作为变量,并分析它们的基因表达谱。

结果
本项研究发现来自CD患者的Treg细胞表达的整合素α4β7水平低于对照患者的Treg细胞。调节整联蛋白亚基α表达的途径由维甲酸受体(RA)诱导。与用雷帕霉素或雷帕霉素联合全反式维甲酸受体培养的细胞相比,来自用雷帕霉素和RARA激动剂(RAR568)孵育的CD患者的Treg细胞表达高水平的整合素α4β7,以及CD62L和FOXP3。RAR568对细胞稳定性或谱系定型没有影响。与在对照培养基中扩增的Treg细胞相比,与RAR568一起温育的荧光标记的Treg细胞显着更有可能转运至肠异种移植物。

结论
来自CD患者的Treg细胞表达整合素α4β7的水平低于来自对照患者的Treg细胞。用雷帕霉素和RARA激动剂孵育患者体外扩增的Treg细胞诱导α4β7的表达,并且在小鼠的培养和肠异种移植物中具有抑制和迁移活性。

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    2019-06-02 许安
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