Hanekom W A, Hussey G D, Hughes E J, Potgieter S, Yogev R, Check I J
Division of Pediatric Infectious Diseases, Northwestern University Medical School, Chicago, Illinois 60614, USA.
Clin Diagn Lab Immunol. 1999 Mar;6(2):204-8. doi: 10.1128/CDLI.6.2.204-208.1999.
Plasma-soluble CD30 (sCD30) is the result of proteolytic splicing from the membrane-bound form of CD30, a putative marker of type 2 cytokine-producing cells. We measured sCD30 levels in children with tuberculosis, a disease characterized by prominent type 1 lymphocyte cytokine responses. We postulated that disease severity and nutritional status would alter cytokine responses and therefore sCD30 levels. Samples from South African children enrolled prospectively at the time of diagnosis of tuberculosis were analyzed. (Patients were originally enrolled in a randomized, double-blind placebo-controlled study of the effects of oral vitamin A supplementation on prognosis of tuberculosis.) Plasma samples collected at the time of diagnosis and 6 and 12 weeks later (during antituberculosis therapy) were analyzed. sCD30 levels were measured by enzyme immunoassay. The 91 children included in the study demonstrated high levels of sCD30 at diagnosis (median, 98 U/liter; range, 11 to 1,569 U/liter). Although there was a trend toward higher sCD30 levels in more severe disease (e.g., culture-positive disease or miliary disease), this was not statistically significant. Significantly higher sCD30 levels were demonstrated in the presence of nutritional compromise: the sCD30 level was higher in patients with a weight below the third percentile for age, in those with clinical signs of kwashiorkor, and in those with a low hemoglobin content. There was minimal change in the sCD30 level after 12 weeks of therapy, even though patients improved clinically. However, changes in sCD30 after 12 weeks differed significantly when 46 patients (51%) who received vitamin A were compared with those who had received a placebo. Vitamin A-supplemented children demonstrated a mean (+/- standard error of the mean) decrease in sCD30 by a factor of 0.99 +/- 0.02 over 12 weeks, whereas a factor increase of 1.05 +/- 0.02 was demonstrated in the placebo group (P = 0.02). We conclude that children with tuberculosis had high sCD30 levels, which may reflect the presence of a type 2 cytokine response. Nutritional compromise was associated with higher sCD30 levels. Vitamin A therapy resulted in modulation of sCD30 levels over time.
血浆可溶性CD30（sCD30）是CD30膜结合形式经蛋白水解剪接后的产物，CD30是2型细胞因子产生细胞的一种假定标志物。我们检测了结核病患儿的sCD30水平，结核病是以突出的1型淋巴细胞细胞因子反应为特征的疾病。我们推测疾病严重程度和营养状况会改变细胞因子反应，进而影响sCD30水平。对前瞻性纳入的南非结核病诊断患儿的样本进行了分析。（患者最初纳入一项关于口服维生素A补充剂对结核病预后影响的随机、双盲、安慰剂对照研究。）分析了诊断时以及6周和12周后（抗结核治疗期间）采集的血浆样本。通过酶免疫测定法检测sCD30水平。纳入研究的91名儿童在诊断时sCD30水平较高（中位数为98 U/升；范围为11至1569 U/升）。虽然在病情较重的疾病（如培养阳性疾病或粟粒性疾病）中sCD30水平有升高趋势，但差异无统计学意义。在存在营养缺陷的情况下，sCD30水平显著升高：年龄体重低于第3百分位数的患者、有夸希奥科病临床体征的患者以及血红蛋白含量低的患者，其sCD30水平更高。治疗12周后，尽管患者临床症状有所改善，但sCD30水平变化极小。然而，将46名（51%）接受维生素A治疗的患者与接受安慰剂治疗的患者相比，12周后sCD30的变化有显著差异。补充维生素A的儿童在12周内sCD30平均（±平均标准误）下降了0.99±0.02倍，而安慰剂组则升高了1.05±0.02倍（P = 0.02）。我们得出结论，结核病患儿的sCD30水平较高，这可能反映了2型细胞因子反应的存在。营养缺陷与较高的sCD30水平相关。维生素A治疗导致sCD30水平随时间发生调节。
