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Differential Effects of Control and Antigen-Specific T Cells on Intracellular Mycobacterial Growth

机译：对照和抗原特异性T细胞对细胞内分枝杆菌生长的差异作用

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We investigated the effects of peripheral blood mononuclear cells expanded with irrelevant control and mycobacterial antigens on the intracellular growth of Mycobacterium bovis bacillus Calmette-Guérin (BCG) in human macrophages. More than 90% of the cells present after 1 week of in vitro expansion were CD3+. T cells were expanded from purified protein derivative-negative controls, persons with latent tuberculosis, and BCG-vaccinated individuals. T cells expanded with nonmycobacterial antigens enhanced the intracellular growth of BCG in suboptimal cultures of macrophages. T cells expanded with live BCG or lysates of Mycobacterium tuberculosis directly inhibited intracellular BCG. Recent intradermal BCG vaccination significantly enhanced the inhibitory activity of T cells expanded with mycobacterial antigens (P < 0.02), consistent with the induction of memory-immune inhibitory T-cell responses. Selected mycobacterial antigens (Mtb41 > lipoarabinomannan > 38kd > Ag85B > Mtb39) expanded inhibitory T cells, demonstrating the involvement of antigen-specific T cells in intracellular BCG inhibition. We studied the T-cell subsets and molecular mechanisms involved in the memory-immune inhibition of intracellular BCG. Mycobacteria-specific γδ T cells were the most potent inhibitors of intracellular BCG growth. Direct contact between T cells and macrophages was necessary for the BCG growth-enhancing and inhibitory activities mediated by control and mycobacteria-specific T cells, respectively. Increases in tumor necrosis factor alpha, interleukin-6, transforming growth factor β, and vascular endothelial growth factor mRNA expression were associated with the enhancement of intracellular BCG growth. Increases in gamma interferon, FAS, FAS ligand, perforin, granzyme, and granulysin mRNA expression were associated with intracellular BCG inhibition. These culture systems provide in vitro models for studying the opposing T-cell mechanisms involved in mycobacterial survival and protective host immunity.
机译：我们调查了不相关控制和分枝杆菌抗原扩增的外周血单核细胞对人巨噬细胞中牛分枝杆菌卡介苗的细胞内生长的影响。体外扩增1周后，存在的细胞中90％以上是CD3 + 。 T细胞从纯化的蛋白衍生物阴性对照，潜伏性结核病患者和BCG疫苗接种者中扩增。用非分枝杆菌抗原扩增的T细胞在巨噬细胞的次优培养中增强了BCG的细胞内生长。 T细胞与活卡介苗或结核分枝杆菌的溶解产物一起扩增可直接抑制细胞内卡介苗。最近的真皮内BCG疫苗接种显着增强了分枝杆菌抗原（ P <0.02）扩展的T细胞的抑制活性，与诱导记忆免疫抑制性T细胞反应一致。选定的分枝杆菌抗原（Mtb41>脂质阿拉伯甘露聚糖> 38kd> Ag85B> Mtb39）扩展了抑制性T细胞，表明抗原特异性T细胞参与了细胞内BCG抑制。我们研究了参与细胞内BCG记忆免疫抑制的T细胞亚群和分子机制。分枝杆菌特异性γδT细胞是细胞内BCG生长的最有效抑制剂。 T细胞和巨噬细胞之间的直接接触对于分别由对照和分枝杆菌特异性T细胞介导的BCG生长和抑制活性是必需的。肿瘤坏死因子α，白介素6，转化生长因子β和血管内皮生长因子mRNA表达的增加与细胞内BCG生长的增强有关。 γ干扰素，FAS，FAS配体，穿孔素，颗粒酶和颗粒溶素mRNA表达的增加与细胞内BCG抑制有关。这些培养系统提供了体外模型，用于研究与分枝杆菌存活和保护性宿主免疫有关的相反的T细胞机制。

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