转铁蛋白增强人CD8 + T细胞的IL-2诱导杀伤活性和穿孔素生成。
Augmentation by transferrin of IL-2-inducible killer activity and perforin production of human CD8+ T cells.
作者信息
Nakamura A, Sone S, Nabioullin R, Sugihara K, Munekata M, Nishioka Y, Nii A, Ogura T
机构信息
Third Department of Internal Medicine, University of Tokushima School of Medicine, Japan.
出版信息
Clin Exp Immunol. 1993 Apr;92(1):174-9. doi: 10.1111/j.1365-2249.1993.tb05966.x.
The effects of human transferrin (Tf) on lymphokine (IL-2)-activated killer (LAK) induction from blood lymphocytes of healthy donors was examined. LAK cells were induced by 6-day incubation in medium with recombinant human IL-2 of lymphocytes, and their cytotoxic activity was assessed by measuring 51Cr release from NK-resistant Daudi cells. Tf alone did not induce any LAK activity, but in combination with IL-2, it augmented LAK induction dose- and time-dependently. This augmenting effect was completely abolished by pretreatment with anti-Tf antiserum. Tf augmented the proliferative response of lymphocytes to IL-2 and their expressions of receptors for IL-2 and Tf. CD8+ T cells were isolated from purified blood lymphocytes using antibody-bound magnetic beads. Addition of Tf to cultures of CD8+ cells resulted in significant augmentation of killer cell induction and perforin (PFP) production after 4 days stimulation with IL-2. These results indicate that Tf is important in generation of IL-2-inducible killer properties and PFP activity of human CD8+ T cells.
研究了人转铁蛋白（Tf）对健康供体血液淋巴细胞诱导淋巴因子（IL-2）激活的杀伤细胞（LAK）的影响。LAK细胞通过在含有重组人IL-2的培养基中培养淋巴细胞6天诱导产生，其细胞毒性活性通过测量NK抗性Daudi细胞的51Cr释放来评估。单独的Tf不诱导任何LAK活性，但与IL-2联合使用时，它以剂量和时间依赖性方式增强LAK诱导。用抗Tf抗血清预处理可完全消除这种增强作用。Tf增强了淋巴细胞对IL-2的增殖反应及其IL-2和Tf受体的表达。使用抗体结合的磁珠从纯化的血液淋巴细胞中分离出CD8 + T细胞。在IL-2刺激4天后，向CD8 +细胞培养物中添加Tf导致杀伤细胞诱导和穿孔素（PFP）产生显著增强。这些结果表明，Tf在人CD8 + T细胞的IL-2诱导杀伤特性和PFP活性的产生中起重要作用。
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