Vγ1+ γδ T cells reduce IL-10-producing CD4+CD25+ T cells in the lung of ovalbumin-sensitized and challenged mice.
Vγ1+ γδ T cells reduce IL-10-producing CD4+CD25+ T cells in the lung of ovalbumin-sensitized and challenged mice.
复制标题
Vγ1+γδT细胞减少了产生IL-10的CD4+ CD25+ T细胞，卵巢蛋白敏感和挑战小鼠的肺中。
DOI：
10.1016/j.imlet.2008.09.001
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发表时间：
2008-12-22
影响因子：
4.4
通讯作者：
Born WK
中科院分区：
文献类型：
--
作者：
Hahn YS;Ji XY;Woo SI;Choi YK;Song MS;Shin KS;Jin N;O'Brien RL;Born WK
在OVA致敏和激发的小鼠中，表达Vγ1的γδ T细胞增强气道高反应性（AHR），但其潜在机制尚不清楚。这些细胞还降低气道中的IL-10水平，表明它们可能通过抑制CD 4 + CD 25+调节性T细胞（Treg）或能够产生IL-10和抑制AHR的其他CD 4 + T细胞来发挥作用。事实上，用OVA致敏和激发结合Vγ1+细胞灭活增加了肺中的CD 4 + CD 25+细胞，并且显著增加了那些能够产生IL-10的细胞。细胞变化与气道中IL-10和TGF-β水平升高以及IL-13降低相关。Treg包括天然存在的Foxp 3 + Treg、诱导型Foxp 3 − Treg和抗原特异性Treg，其中许多表达叶酸受体4（FR 4）。虽然Foxp 3基因在肺中的表达也增加了肺CD 4 + T细胞，但表达Foxp 3蛋白或FR 4的细胞保持稳定。因此，Vγ1+ γδ T细胞的抑制可能不靶向Foxp 3 + Treg，而是靶向注定产生IL-10的CD 4 + T细胞。
In OVA-sensitized and challenged mice, γδ T cells expressing Vγ1 enhance airway hyperresponsiveness (AHR) but the underlying mechanism is unclear. These cells also reduce IL-10 levels in the airways, suggesting that they might function by inhibiting CD4+CD25+ regulatory T cells (Treg) or other CD4+ T cells capable of producing IL-10 and suppressing AHR. Indeed, sensitization and challenge with OVA combined with inactivation of Vγ1+ cells increased CD4+CD25+ cells in the lung, and markedly those capable of producing IL-10. The cellular change was associated with increased IL-10 and TGF-β levels in the airways, and a decrease of IL-13. Treg include naturally occurring Foxp3+ Treg, inducible Foxp3− Treg, and antigen-specific Treg many of which express folate receptor 4 (FR4). Although Foxp3 gene expression in the lung was also increased pulmonary CD4+ T cells, expressing Foxp3-protein or FR4 remained stable. Therefore, the inhibition by Vγ1+ γδ T cells might not be targeting Foxp3+ Treg but rather CD4+ T cells destined to produce IL-10.