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首页> 美国卫生研究院文献>Immunology >Differential effects of pentoxifylline on the production of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) by monocytes and T cells.
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Differential effects of pentoxifylline on the production of tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) by monocytes and T cells.

机译：己酮可可碱对单核细胞和T细胞产生肿瘤坏死因子-α（TNF-α）和白介素6（IL-6）的差异作用。

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Pentoxifylline (PTX) is a methylxanthine compound known to inhibit the production of tumour necrosis factor-alpha (TNF-alpha) by monocytic cells. In this study, we found that PTX differentially regulates the production of TNF-alpha and interleukin-6 (IL-6). Indeed, PTX at high concentrations triggers the production of IL-6 but not of TNF-alpha by peripheral blood mononuclear cells (PBMC). Further experiments indicated that monocytes are responsible for this PTX-induced IL-6 production. When PBMC were stimulated with LPS, PTX was found to inhibit the secretion of TNF-alpha as well as the accumulation of TNF-alpha messenger RNA (mRNA). In contrast, no inhibitory effect was observed on the induction of IL-6. Similar results were obtained when PBMC were stimulated with OKT3 monoclonal antibody (mAb). In addition, the in vivo administration of PTX in transplant patients receiving the first dose of OKT3 allowed to decrease the systemic release of TNF-alpha but not of IL-6. Since monocytes represent a major source of TNF-alpha and IL-6 in these settings, additional experiments were performed in vitro on purified T cells stimulated with the CLB-T3/3, an anti-CD3 mAb which does not require the presence of accessory cells to activate T cells. In this system, PTX was found to inhibit the secretion of both TNF-alpha and IL-6 by T cells. We suggest that cAMP could be involved in these differential effects of PTX on production of TNF-alpha and of IL-6.
机译：己酮可可碱（PTX）是一种甲基黄嘌呤化合物，已知可抑制单核细胞产生肿瘤坏死因子-α（TNF-α）。在这项研究中，我们发现PTX差异性调节TNF-α和白介素6（IL-6）的产生。实际上，高浓度的PTX会触发外周血单核细胞（PBMC）产生IL-6，但不会触发TNF-α。进一步的实验表明，单核细胞是造成PTX诱导的IL-6产生的原因。当用LPS刺激PBMC时，发现PTX抑制TNF-α的分泌以及TNF-α信使RNA（mRNA）的积累。相反，未观察到对IL-6诱导的抑制作用。用OKT3单克隆抗体（mAb）刺激PBMC可获得相似的结果。另外，在接受第一剂OKT3的移植患者中体内给予PTX可以减少TNF-α的全身释放，但不能减少IL-6的全身释放。由于在这些情况下单核细胞是TNF-α和IL-6的主要来源，因此在体外用CLB-T3 / 3（一种不需要附件的抗CD3 mAb）刺激的纯化T细胞进行了其他实验细胞激活T细胞。在该系统中，发现PTX抑制T细胞分泌TNF-α和IL-6。我们建议cAMP可能参与PTX对TNF-α和IL-6产生的这些差异作用。

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