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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Pentoxifylline down-regulates adhesion molecule expression and inflammatory cytokine production in cultured peripheral blood mononuclear cells from patients with HTLV-I-associated myelopathy.
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Pentoxifylline down-regulates adhesion molecule expression and inflammatory cytokine production in cultured peripheral blood mononuclear cells from patients with HTLV-I-associated myelopathy.

机译：己酮可可碱下调HTLV-I相关性脊髓病患者外周血单个核细胞中粘附分子的表达和炎性细胞因子的产生。

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摘要

To clarify if pentoxifylline (PTX) may have therapeutic potential for human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM), we investigated the in vitro effect of PTX on spontaneous proliferation of peripheral blood lymphocytes (SPP), as well as on the expression of adhesion molecules, such as lymphocyte function antigen-1 (LFA-1) and very late activation antigen-4 (VLA-4), and the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and granulocyte-monocyte colony stimulating factor (GM-CSF), in cultured PBMC from 10 HAM patients, compared with control subjects. SPP in HAM patients was significantly suppressed in a dose-dependent manner with PTX. Using flow cytometry, PTX was found to down-regulate the expression of LFA-1 and VLA-4 on CD4+ and CD8+ T cells in HAM patients as well as control subjects. However, the fall in the expression of LFA-1 and VLA-4 on CD4+ T cell population in HAM patients was higher than that of control subjects. PTX caused a significant suppression of spontaneous production of TNF-alpha by cultured PBMC of HAM patients. It also caused a small but significant suppression GM-CSF and IFN-gamma production. Collectively, our results suggest that PTX might be therapeutically effective at critical points in the immunopathogenesis of HAM.
机译：为了阐明己酮可可碱（PTX）是否可能具有治疗人类I型T细胞淋巴病毒（HTLV-1）相关性脊髓病（HAM）的潜力，我们调查了PTX对外周血淋巴细胞（SPP）自发增殖的体外作用，以及黏附分子的表达，例如淋巴细胞功能抗原1（LFA-1）和极晚期活化抗原4（VLA-4），以及炎性细胞因子的产生，例如肿瘤坏死因子-α与对照组相比，来自10例HAM患者的培养的PBMC中的TNF-α，干扰素-γ（IFN-γ）和粒细胞-单核细胞集落刺激因子（GM-CSF）。 PTX以剂量依赖的方式显着抑制了HAM患者的SPP。使用流式细胞仪，发现PTX下调HAM患者和对照组受试者CD4 +和CD8 + T细胞上LFA-1和VLA-4的表达。但是，HAM患者CD4 + T细胞群体中LFA-1和VLA-4的表达下降高于对照组。 PTX通过培养HAM患者的PBMC显着抑制了TNF-α的自发产生。它还引起了少量但明显的GM-CSF和IFN-γ抑制。总的来说，我们的结果表明PTX可能在HAM免疫发病机理的关键点上具有治疗效果。

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