Abe Y, Kimura K, Horiuchi A, Watanabe Y, Kimura S
Second Department of Surgery, Ehime University School of Medicine, Japan.
Surg Today. 1994;24(6):506-11. doi: 10.1007/BF01884569.
Soluble tumor necrosis factor receptor (sTNF-R) is known to inhibit patient immunity via specific binding with the TNF molecule. To examine the possible involvement of sTNF-R in cancer immunotherapy, the plasma levels of sTNF-R of both 55 kDa and 75 kDa origins were estimated when TNF was induced in patients with malignancy using both a polysaccharide preparation (Lentinan) and a streptococcal preparation (OK-432). The pretreatment plasma levels of the 55 kDa and 75 kDa sTNF-R were 1.04 +/- 0.53 and 1.06 +/- 0.34 ng/ml (mean +/- SE), respectively. The plasma levels of TNF were undetectable before treatment. The plasma sTNF-R levels peaked 2 h after the administration of OK-432 and followed the same pattern as the TNF levels in plasma. Both TNF and sTNF-R nearly returned to pretreatment levels at 16 h after the induction of TNF. The peak plasma levels of the 55 kDa and 75 kDa sTNF-R were 2.46 +/- 0.95 and 3.03 +/- 0.88 ng/ml, respectively, but they did not correlate with the plasma TNF levels. When peripheral white blood cells were cultured with the addition of lipopolysaccharide in vitro, an elevation of the 72 kDa sTNF-R was detected. Thus, the plasma source of this soluble receptor can at least be partly attributed to the white blood cells. However, the 55 kDa sTNF-R showed little increase in the cultures, and its source remains unknown. We should therefore be aware of the elevation of plasma sTNF-R levels by the induction therapy of TNF for patients with malignancies because of the immunosuppressive effect of sTNF-R.
可溶性肿瘤坏死因子受体（sTNF-R）已知可通过与TNF分子特异性结合来抑制患者的免疫力。为了研究sTNF-R在癌症免疫治疗中的可能作用，在使用多糖制剂（香菇多糖）和链球菌制剂（OK-432）诱导恶性肿瘤患者体内产生TNF时，对55 kDa和75 kDa来源的sTNF-R的血浆水平进行了评估。55 kDa和75 kDa sTNF-R的预处理血浆水平分别为1.04±0.53和1.06±0.34 ng/ml（平均值±标准误）。治疗前血浆中未检测到TNF水平。在给予OK-432后2小时，血浆sTNF-R水平达到峰值，并且与血浆中TNF水平的变化模式相同。在诱导TNF后16小时，TNF和sTNF-R的水平几乎都恢复到了预处理水平。55 kDa和75 kDa sTNF-R的血浆峰值水平分别为2.46±0.95和3.03±0.88 ng/ml，但它们与血浆TNF水平不相关。当在体外培养外周血白细胞并添加脂多糖时，检测到72 kDa sTNF-R升高。因此，这种可溶性受体的血浆来源至少部分可归因于白细胞。然而，55 kDa sTNF-R在培养物中几乎没有增加，其来源仍然未知。因此，由于sTNF-R的免疫抑制作用，我们应该意识到对于恶性肿瘤患者，TNF诱导疗法会导致血浆sTNF-R水平升高。
