In vitro maturation of human neonatal CD4 T lymphocytes. II. Cytokines present at priming modulate the development of lymphokine production.
In vitro maturation of human neonatal CD4 T lymphocytes. II. Cytokines present at priming modulate the development of lymphokine production.
复制标题
人新生儿 CD4 T 淋巴细胞的体外成熟。
作者：
C. E. Demeure;Chang;U. Shu;P. Schneider;C. Heusser;H. Yssel;G. Delespesse
幼稚CD 4 T细胞发育为1型或2型Th细胞已在小鼠中进行了广泛分析。使用新生儿CD 4 T淋巴细胞作为人类幼稚细胞的来源，我们报告说，这些细胞可以诱导分化为效应细胞主要产生Th 1或Th 2细胞因子。用固定在CD 32转染的小鼠成纤维细胞上的抗CD 3 mAb刺激3天后，接着在IL-2存在下培养3天，新生细胞获得效应细胞的表型和功能特征。致敏的细胞富含CD 45 R 0 hi和CD 31-细胞，并且在用PMA+离子霉素刺激后，它们释放显著量的IL-2、IFN-γ、IL-4、IL-5和IL-10。在用抗-CD 3活化期间加入外源性细胞因子显著改变了由致敏细胞产生的细胞因子的概况：1）IL-2均匀地增强Th 1和Th 2细胞因子的产生; 2）IL-4显著地增强IL-4、IL-5和IL-10的释放，并抑制IFN-γ的释放; 3）IFN-γ强烈地抑制IL-4和IL-5的产生，但轻微地增强IFN-γ的释放; 4）IFN-α显著地抑制IL-4和IL-5的产生，并增加IFN-γ和IL-10的产生; 5）TGF-β抑制IL-4和IL-5（以及在较小程度上抑制IL-2）产生，但对IL-10和IFN-γ产生具有不一致的作用。外源性细胞因子的这些作用与致敏细胞上CD 31表达的改变无关。
The development of naive CD4 T cells into type 1 or type 2 Th cells has been extensively analyzed in the mouse. Using neonatal CD4 T lymphocytes as a source of human naive cells, we report that these cells may be induced to differentiate into effector cells producing predominantly Th1 or Th2 cytokines. After 3 days of stimulation with anti-CD3 mAb immobilized on CD32 transfected mouse fibroblasts, followed by 3 days of culture in the presence of IL-2, neonatal cells acquire the phenotypic and functional characteristics of effector cells. Primed cells are enriched in CD45R0hi and CD31- cells, and upon stimulation with PMA+ ionomycin they release significant amounts of IL-2, IFN-gamma, IL-4, IL-5, and IL-10. Addition of exogenous cytokines during the period of activation with anti-CD3 markedly alters the profile of cytokine production by primed cells: 1) IL-2 uniformly enhances Th1 and Th2 cytokine production; 2) IL-4 markedly enhances the release of IL-4, IL-5, and IL-10 and suppresses that of IFN-gamma; 3) IFN-gamma strongly inhibits IL-4 and IL-5 production but slightly enhances IFN-gamma release; 4) IFN-alpha markedly inhibits IL-4 and IL-5 production and increases the production of both IFN-gamma and of IL-10; 5) TGF-beta suppresses IL-4 and IL-5 (and to a lesser extent IL-2) production but has inconsistent effect on IL-10 and IFN-gamma production. These effects of exogenous cytokines are not associated with an alteration of CD31 expression on primed cells.