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首页> 外文期刊>Infection and immunity >A monoclonal antibody that recognizes phosphatidylinositol inhibits induction of tumor necrosis factor alpha by different strains of Plasmodium falciparum.
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A monoclonal antibody that recognizes phosphatidylinositol inhibits induction of tumor necrosis factor alpha by different strains of Plasmodium falciparum.

机译：识别磷脂酰肌醇的单克隆抗体可抑制恶性疟原虫不同菌株对肿瘤坏死因子α的诱导。

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摘要

The clinical symptoms of human malaria are mediated, at least in part, by the release of tumor necrosis factor alpha (TNF) by monocytes and macrophages. We have found that lysates of Plasmodium falciparum-infected erythrocytes stimulate the secretion of TNF from human mononuclear cells, and we have generated several immunoglobulin M monoclonal antibodies (MAbs) that inhibit the induction of TNF by such lysates. Here we describe the properties of MAb 5AB3-11, which causes dose-dependent inhibition of the TNF-inducing factors derived from P. falciparum-infected erythrocytes, with a 50% reduction in TNF secretion at nanomolar concentrations (1 to 2 micrograms/ml). The inhibitory effect appears to be malaria specific in that the induction of TNF by either lipopolysaccharide or lipoteichoic acid is not affected. MAb 5AB3-11 binds to liposomes containing phosphatidylinositol but not to other phospholipid liposomes, showing that it recognizes a phosphatidylinositol-like epitope. MAb 5AB3-11 inhibits the induction of TNF by whole lysates from several strains of P. falciparum which originated from different parts of the tropics, indicating that all of the major TNF-inducing factors derived from Plasmodium-infected erythrocytes contain a common epitope. A phosphatidylinositol-like epitope expressed by Plasmodium-infected erythrocytes may be a suitable immunological target for the prevention or treatment of severe malaria.
机译：人类疟疾的临床症状至少部分地由单核细胞和巨噬细胞释放肿瘤坏死因子α（TNF）介导。我们发现恶性疟原虫感染的红细胞的裂解物刺激人单核细胞分泌TNF，并且我们已经产生了几种免疫球蛋白M单克隆抗体（MAb），它们抑制了这种裂解物对TNF的诱导。在这里我们描述了单克隆抗体5AB3-11的特性，该特性导致剂量依赖性抑制源自恶性疟原虫感染的红细胞的TNF诱导因子，在纳摩尔浓度下（1-2微克/毫升）TNF分泌减少50％ ）。抑制作用似乎是疟疾特有的，因为脂多糖或脂磷壁酸对TNF的诱导不受影响。 MAb 5AB3-11与包含磷脂酰肌醇的脂质体结合，但不与其他磷脂脂质体结合，表明它识别磷脂酰肌醇样表位。 MAb 5AB3-11抑制了来自热带不同地区的几种恶性疟原虫菌株的整体裂解液对TNF的诱导，这表明源自疟原虫感染的红细胞的所有主要TNF诱导因子均包含一个共同的表位。由疟原虫感染的红细胞表达的磷脂酰肌醇样表位可能是预防或治疗严重疟疾的合适免疫学靶标。

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