Matured in the thymus, γδT cells can modulate the development of allergy in humans. The main γδT cell subsets have been described as interleukin (IL)-17A or interferon (IFN)-γ producers, but these cells can also produce other modulatory cytokines, such as IL-4 and IL-10. Here, we aimed to evaluate whether IgG can modulate the profile of cytokine production by γδT cells during their maturation in the thymus and after its migration to peripheral tissues. Thymic tissues were obtained from 12 infants, and peripheral blood mononuclear cells (PBMCs) were obtained from adults (both groups without an atopic background). IgG was purified from atopic and non-atopic volunteers. Thymocytes and PBMCs were cultured with purified atopic or non-atopic IgG, and intracellular cytokine production and phenotype were assessed. Mock and IVIg conditions were used as controls. IgG from non-atopic individuals induced IFN-γ and IL-10 production by thymic γδT cells, and no effect was observed on peripheral γδT cells. IL-17 production was inhibited by non-atopic IgG on thymic γδT cells and augmented by atopic IgG on peripheral γδT cells. Modulated thymic γδT cells did not produce IFN-γ and IL-10 simultaneously. We additionally evaluated the phenotype of intrathymic γδT cells and observed that IgG from all groups could induce CD25 expression and could not influence the CD28 expression of these cells. This report describes evidence revealing that IgG may influence the production of IFN-γ and IL-10 by intrathymic γδT cells depending on the donor atopic state. This observation is unprecedented and needs to be considered in further studies in the IgG immunotherapy field.

中文翻译：

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来自非特应性个体的IgG诱导人胸腺γδT细胞体外产生IFN-γ和IL-10：与特应性IgG和IVIg的比较。

γδT细胞在胸腺中成熟，可以调节人类过敏的发展。γδT细胞的主要子集已被描述为白介素（IL）-17A或干扰素（IFN）-γ的产生者，但这些细胞还可以产生其他调节性细胞因子，例如IL-4和IL-10。在这里，我们旨在评估IgG是否能调节γδT细胞在胸腺成熟过程中以及迁移到周围组织后γδT细胞产生的细胞因子。胸腺组织取自12例婴儿，外周血单核细胞（PBMC）取自成人（两组均无特应性背景）。从特应性和非特应性志愿者中纯化IgG。用纯化的特应性或非特应性IgG培养胸腺细胞和PBMC，并评估细胞内细胞因子的产生和表型。模拟和IVIg条件用作对照。来自非特应性个体的IgG诱导胸腺γδT细胞产生IFN-γ和IL-10，并且未观察到对外周γδT细胞的影响。IL-17的产生被胸腺γδT细胞上的非特应性IgG抑制，并被外周γδT细胞上的异应性IgG增强。胸腺γδT调节细胞不能同时产生IFN-γ和IL-10。我们还评估了胸腺内γδT细胞的表型，并观察到所有组的IgG均可诱导CD25表达，而不会影响这些细胞的CD28表达。该报告描述的证据表明，IgG可能会影响胸腺内γδT细胞的IFN-γ和IL-10的产生，具体取决于供体的异位状态。这种观察是前所未有的，需要在IgG免疫治疗领域的进一步研究中加以考虑。来自非特应性个体的IgG诱导胸腺γδT细胞产生IFN-γ和IL-10，并且未观察到对外周γδT细胞的影响。胸腺γδT细胞上的非特应性IgG抑制了IL-17的产生，而外周γδT细胞上的特应性IgG增强了IL-17的产生。胸腺γδT调节细胞不能同时产生IFN-γ和IL-10。我们还评估了胸腺内γδT细胞的表型，并观察到所有组的IgG均可诱导CD25表达，而不会影响这些细胞的CD28表达。该报告描述的证据表明，IgG可能会影响胸腺内γδT细胞的IFN-γ和IL-10的产生，具体取决于供体的异位状态。这种观察是前所未有的，需要在IgG免疫治疗领域的进一步研究中加以考虑。来自非特应性个体的IgG诱导胸腺γδT细胞产生IFN-γ和IL-10，并且未观察到对外周γδT细胞的影响。IL-17的产生被胸腺γδT细胞上的非特应性IgG抑制，并被外周γδT细胞上的异应性IgG增强。胸腺γδT调节细胞不能同时产生IFN-γ和IL-10。我们还评估了胸腺内γδT细胞的表型，并观察到所有组的IgG均可诱导CD25表达，而不会影响这些细胞的CD28表达。该报告描述的证据表明，IgG可能会影响胸腺内γδT细胞的IFN-γ和IL-10的产生，具体取决于供体的异位状态。这种观察是前所未有的，需要在IgG免疫治疗领域的进一步研究中加以考虑。