哮喘患者调节性T细胞对Th1和Th2细胞的影响

Effect of T-regulatory cells on helper T1 and helper T2 cells in asthmatic patients

目的探讨轻、中度哮喘患者急性发作期调节性T细胞(T-regulatory cells,Tregs)对辅助性T细胞(helper T cell,Th)1、Th2细胞功能的影响。方法采集30例轻、中度哮喘急性发作期患者(哮喘组)和30例同期体检健康者(对照组)外周静脉血,分离单个核细胞(peripheral blood mononuclear cell,PBMC),应用磁珠法体外分离CD4+CD25+CD127-/low T细胞和CD4+CD25-T细胞,体外培养,观察Tregs对效应细胞增殖及Th1、Th2分化的影响。结果 (1)哮喘组CD4+CD25+CD127-/low/PBMC比率[(2.26±0.14)%]以及CD4+CD25+CD127-/low T细胞对CD4+CD25-T细胞的抑制率(52.92%)均低于对照组[(3.04±0.18)%,85.51%](P<0.05);(2)哮喘组Tregs对GATA-3基因、白细胞介素-13的抑制率(27.06%,56.34%)低于对照组(79.60%,86.73%)(P<0.05);(3)经Tregs干预,哮喘组T-bet/GATA-3比值(0.54±0.11)低于非Tregs干预(0.78±0.16)(P<0.05)。结论轻、中度哮喘急性发作期患者Tregs数量及功能均下降;Tregs对效应T细胞及Th2细胞的抑制作用降低可能是导致Th1/Th2细胞轴偏向于Th2细胞极性发展的原因。

Objective To study the effect of T-regulatory cells （Tregs） on helper T1 and T2 cells in patients with mild to moderate asthma in accute attack period. Methods The peripheral blood mononuclear cells （PBMCs） were isolated from 30 mild to moderate asthmatic patients in acute attack stage （asthma group） and 30 healthy controls （control group）. CD4＋ CD25＋ CD127 /low Tregs and CD4＋ CD25- T cells from PBMCs were isolated by immunomagnetic beads method and cultured in vitro to observe the effector cells proliferation and the influence of Tregs on Thl and Th2 cells. Results The ratio of CD4＋ CD25＋ CD127-/low/PBMC and the suppressive rate of CD4＋ CD25＋ CD127-/low T on CD4＋ CD25- T were lower in asthma group （（2.26±0. 14）%, 52. 92%） than those in control group （（3. 04±0. 18）%, 85. 51%） （P〈 0.05）. The suppressive rate of Tregs on the expression of GATA-3 and interleukin-13 were lower in asthma group （27.06 %, 56.34%） than those in control group （79.60%, 86.73%） （P〈0.05）. The ratio of T-bet/GATA-3 was lower in asthma group （0.54±0.11） than that in control group （0.78±0.16） （P〈0.05）. Conclusion The number and the suppressive capacity of Tregs decrease in patients with mild to moderate asthma. The decreased suppressive capacity of Tregs on effector T cells and Th2 may induce Th2-polarization in asthma development.