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首页> 外文期刊>Inflammatory bowel diseases >Therapy with anti-TNFalpha antibody enhances number and function of Foxp3(+) regulatory T cells in inflammatory bowel diseases.
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Therapy with anti-TNFalpha antibody enhances number and function of Foxp3(+) regulatory T cells in inflammatory bowel diseases.

机译：抗TNFalpha抗体治疗可增强炎症性肠病中Foxp3（+）调节性T细胞的数量和功能。

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BACKGROUND: Inflammatory bowel diseases (IBDs) are associated with up-regulation of TNFalpha, hyperactivation of proinflammatory effector T cells (Teffs) and inefficient control by regulatory CD4(+) CD25(+) Foxp3(+) T cells (Tregs). The aim of this prospective study was to investigate the short-term impact of treatment of IBD patients with anti-TNFalpha antibodies (infliximab or adalimumab) on the frequency, phenotype, and suppressive function of Tregs. METHODS: Active IBD patients including 16 with Crohn's disease and 9 with ulcerative colitis were treated with anti-TNFalpha mAb. PBMCs were harvested immediately before and 2 weeks after the first injection. The frequency and phenotype of circulating CD4(+) CD25(+) Foxp3(+) Tregs were analyzed by flow cytometry, and their suppressive function was assessed by the ability of purified CD4(+) CD25(+) CD127(-) Tregs to inhibit the proliferation of allogenic CD4(+) CD25(-) Teffs. RESULTS: CD4(+) CD25(+) Foxp3(+) Treg frequency was significantly lower in active IBD patients than in controls (2.8% +/- 0.4% vs. 4.6% +/- 0.6%, respectively; P = 0.01). On day 14 following the first anti-TNFalpha infusion, the frequency of circulating Tregs was significantly enhanced in IBD patients (4.0% +/- 0.5% vs. 2.8% +/- 0.4%, before treatment; P = 0.001), with a 2- to 3-fold increase in the intensity of Foxp3 expression. In addition, infliximab treatment enhanced the suppressive function of circulating Tregs, as shown by inhibition of Teff proliferation at a 1:8 Treg/Teff ratio (28% +/- 5% vs. 66% +/- 10%, after treatment; P = 0.04). CONCLUSIONS: These data demonstrate that anti-TNFalpha treatment of active IBD rapidly enhances the frequency of functional Foxp3(+) Tregs in blood and potentiates their suppressive function. This indicates that Treg potentiation may represent an unanticipated outcome of anti-TNFalpha biotherapy in IBD.
机译：背景：炎症性肠病（IBDs）与TNFalpha的上调，促炎性效应T细胞（Teffs）的过度活化以及CD4（+）CD25（+）Foxp3（+）T细胞（Tregs）的无效控制有关。这项前瞻性研究的目的是研究用抗TNFα抗体（英夫利昔单抗或阿达木单抗）治疗IBD患者对Treg的频率，表型和抑制功能的短期影响。方法：采用抗TNFαmAb治疗活跃的IBD患者，包括16例克罗恩病和9例溃疡性结肠炎。在第一次注射之前和之后两周收获PBMC。流式细胞仪分析循环CD4（+）CD25（+）Foxp3（+）Treg的频率和表型，并通过纯化CD4（+）CD25（+）CD127（-）Treg的能力评估其抑制功能。抑制同种异体CD4（+）CD25（-）Teffs的增殖。结果：活跃IBD患者的CD4（+）CD25（+）Foxp3（+）Treg频率显着低于对照组（分别为2.8％+/- 0.4％和4.6％+/- 0.6％; P = 0.01） 。首次抗TNFα输注后第14天，IBD患者的循环Treg频率显着增加（治疗前为4.0％+/- 0.5％对2.8％+/- 0.4％; P = 0.001）， Foxp3表达强度增加2到3倍。此外，英夫利昔单抗治疗增强了循环中Treg的抑制功能，如治疗后以1：8 Treg / Teff比率抑制Teff增殖所显示（28％+/- 5％对66％+/- 10％; P = 0.04）。结论：这些数据表明抗TNFα治疗活动性IBD迅速增加血液中功能性Foxp3（+）Tregs的频率并增强其抑制功能。这表明Treg增强可能代表IBD中抗TNFalpha生物疗法的意外结果。

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