IgG1抗分枝杆菌抗体可逆转己酮可可碱对分枝杆菌抗原刺激的贴壁细胞分泌的肿瘤坏死因子α（TNF-α）的抑制作用。
IgG1 antimycobacterial antibodies can reverse the inhibitory effect of pentoxifylline on tumour necrosis factor alpha (TNF-alpha) secreted by mycobacterial antigen-stimulated adherent cells.
作者信息
Thakurdas S M, Hasan Z, Hussain R
机构信息
Department of Microbiology, The Aga Khan University, Karachi, Pakistan.
出版信息
Clin Exp Immunol. 2004 May;136(2):320-7. doi: 10.1111/j.1365-2249.2004.02459.x.
Abstract
Chronic inflammation associated with cachexia, weight loss, fever and arthralgia is the hallmark of advanced mycobacterial diseases. These symptoms are attributed to the chronic stimulation of tumour necrosis factor (TNF)-alpha. Mycobacterial components directly stimulate adherent cells to secrete TNF-alpha. We have shown recently that IgG1 antimycobacterial antibodies play a role in augmenting TNF-alpha in purified protein derivative (PPD)-stimulated adherent cells from non-BCG-vaccinated donors. We now show that IgG1 antibodies can also augment TNF-alpha expression in stimulated adherent cells obtained from BCG-vaccinated donors and this augmentation is not linked to interleukin (IL)-10 secretion. In addition IgG1 antimycobacterial antibodies can reverse the effect of TNF-alpha blockers such as pentoxifylline and thalidomide. These studies therefore have clinical implications for anti-inflammatory drug treatments which are used increasingly to alleviate symptoms associated with chronic inflammation.
摘要
与恶病质、体重减轻、发热和关节痛相关的慢性炎症是晚期分枝杆菌病的标志。这些症状归因于肿瘤坏死因子（TNF）-α的慢性刺激。分枝杆菌成分直接刺激黏附细胞分泌TNF-α。我们最近发现，IgG1抗分枝杆菌抗体在增强来自未接种卡介苗供体的纯化蛋白衍生物（PPD）刺激的黏附细胞中TNF-α的产生方面发挥作用。我们现在表明，IgG1抗体也可以增强来自接种卡介苗供体的刺激黏附细胞中TNF-α的表达，并且这种增强与白细胞介素（IL）-10的分泌无关。此外，IgG1抗分枝杆菌抗体可以逆转TNF-α阻滞剂如己酮可可碱和沙利度胺的作用。因此，这些研究对于越来越多地用于减轻与慢性炎症相关症状的抗炎药物治疗具有临床意义。
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