Nazzal D, Gradolatto A, Truffault F, Bismuth J, Berrih-Aknin S
1] INSERM U974, Paris, France [2] CNRS FRE3617, Paris, France [3] Sorbonne Universités, UPMC Univ Paris 06, UM76, Paris, France [4] AIM, Institut de Myologie, Paris, France.
Cell Death Dis. 2014 Sep 11;5(9):e1420. doi: 10.1038/cddis.2014.377.
Natural thymic T regulatory (tTreg) cells maintain tolerance to self-antigen. These cells are generated in the thymus, but how this generation occurs is still controversial. Furthermore, the contribution of thymus epithelial cells to this process is still unclear, especially in humans. Using an exceptional panel of human thymic samples, we demonstrated that medullary thymus epithelial cells (mTECs) promote the generation of tTreg cells and favor their function. These effects were mediated through soluble factors and were mTEC specific since other cell types had no such effect. By evaluating the effects of mTECs on the absolute number of Treg cells and their state of proliferation or cell death, we conclude that mTECs promote the proliferation of newly generated CD25+ cells from CD4+CD25- cells and protect Treg cells from cell death. This observation implicates Bcl-2 and mitochondrial membrane potential changes, indicating that the intrinsic cell death pathway is involved in Treg protection by mTECs. Interestingly, when the mTECs were cultured directly with purified Treg cells, they were able to promote their phenotype but not their expansion, suggesting that CD4+CD25- cells have a role in the expansion process. To explore the mechanisms involved, several neutralizing antibodies were tested. The effects of mTECs on Treg cells were essentially due to interleukin (IL)-2 overproduction by thymus CD4+ T cells. We then searched for a soluble factor produced by mTECs able to increase IL-2 production by CD4+ cells and could identify the inducible T-cell costimulator ligand (ICOSL). Our data strongly suggest a « ménage à trois »: mTEC cells (via ICOSL) induce overproduction of IL-2 by CD25- T cells leading to the expansion of tTreg cells. Altogether, these results demonstrate for the first time a role of mTECs in promoting Treg cell expansion in the human thymus and implicate IL-2 and ICOSL in this process.
天然胸腺调节性T细胞(tTreg)维持对自身抗原的耐受性。这些细胞在胸腺中产生,但这种产生过程的具体机制仍存在争议。此外,胸腺上皮细胞对这一过程的贡献仍不明确,尤其是在人类中。通过使用一组特殊的人类胸腺样本,我们证明了髓质胸腺上皮细胞(mTEC)促进tTreg细胞的产生并有利于其功能。这些作用是通过可溶性因子介导的,并且是mTEC特有的,因为其他细胞类型没有这种作用。通过评估mTEC对Treg细胞绝对数量及其增殖或细胞死亡状态的影响,我们得出结论,mTEC促进从CD4+CD25-细胞新产生的CD25+细胞的增殖,并保护Treg细胞免于细胞死亡。这一观察结果涉及Bcl-2和线粒体膜电位变化,表明内在细胞死亡途径参与了mTEC对Treg细胞的保护。有趣的是,当mTEC与纯化的Treg细胞直接共培养时,它们能够促进其表型但不能促进其扩增,这表明CD4+CD25-细胞在扩增过程中发挥作用。为了探索其中涉及的机制,我们测试了几种中和抗体。mTEC对Treg细胞的作用主要归因于胸腺CD4+T细胞过度产生的白细胞介素(IL)-2。然后,我们寻找一种由mTEC产生的能够增加CD4+细胞IL-2产生的可溶性因子,并鉴定出诱导性T细胞共刺激配体(ICOSL)。我们的数据强烈表明存在一种“三角关系”:mTEC细胞(通过ICOSL)诱导CD25-T细胞过度产生IL-2,从而导致tTreg细胞的扩增。总之,这些结果首次证明了mTEC在促进人类胸腺中Treg细胞扩增中的作用,并表明IL-2和ICOSL参与了这一过程。